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Nephrology — Disease Index & Clinical Criteria

Written by Betra Youhanna, a medical student and not a doctor — check every detail against your own teaching.

Disease Index · 46 entries across 13 categories · deck-derived, finals-triage

Criteria & Scores · 12 staging, scoring, and classification frameworks

C/P — Clinical Presentation
Inves — Investigations
Mng — Management
Special — Pathognomonic / disease-unique

Electrolyte Disorders

4 entries
1

Hypernatraemia

C/P
  • Serum Na > 145 mmol/L → water drawn out of cells → brain shrinks
  • Predominantly neurological symptoms
  • Acute (<48 h): symptomatic — confusion, headache, N/V, seizures, coma
  • Chronic (>48 h): usually asymptomatic (brain adapts by osmotic uptake)
Inves
  • Serum Na — confirm >145 mmol/L threshold
  • Serum + urine osmolality — high serum osm identifies water-loss vs Na-gain
  • Water-loss vs Na-gain workup — ADH status (CDI vs NDI), aldosterone/cortisol if Conn's/Cushing's suspected
Mng
  • Water-loss predominant — 5% dextrose IV or oral water + treat cause (e.g. vasopressin for CDI)
  • Na-gain predominant — diuretics (increase Na loss in urine) + 5% dextrose + treat cause
Special
  • Central DI — ↓ADH from posterior pituitary (idiopathic, trauma, neurosurgery, infection, tumour)
  • Nephrogenic DI — normal ADH but tubules unresponsive (renal disease, sickle cell, lithium)
  • Conn's — adrenal cortex tumour → ↑Na, ↑BP, ↓K, metabolic alkalosis
  • Cushing's — cortisol mineralocorticoid effect (adrenal tumour or corticosteroid intake)
  • Water-loss causes (beyond DI) — insensible loss (sweating, burns, fever, exercise), GI loss (vomiting, diarrhoea), osmotic diuresis (DKA, diuretics)
2

Hyponatraemia

C/P
  • Serum Na < 136 mmol/L → water drawn into cells → brain swells
  • Acute (<48 h): confusion, headache, N/V, seizures, coma
  • Chronic (>48 h): usually asymptomatic (brain excretes intracellular osmoles)
  • Severe (<120 mmol/L) — symptomatic regardless of acute or chronic
Inves
  • Serum Na — confirm <136 mmol/L
  • Serum osmolality — ↓ in true (hypo-osmolar) hyponatraemia
  • Assess volume status first — hypovolaemic / euvolemic / hypervolemic drives the workup
  • Urine Na + osmolality — helps localise SIADH vs renal loss
  • TFTs / short synacthen — rule out hypothyroidism, Addison's
Mng
  • Symptomatic → 3% hypertonic saline (regardless of volume)
  • Asymptomatic hypovolaemic → 0.9% normal saline + treat cause
  • Asymptomatic euvolemic / hypervolemic → water restriction + diuretics + treat cause
Special
  • Hypovolaemic — diuretics, Addison's (↓aldosterone → renal Na loss + hyperkalaemia + metabolic acidosis), vomiting/diarrhoea
  • Euvolemic — SIADH (CNS/pulmonary disease, cancers, SSRIs/TCAs), hypothyroidism, psychogenic polydipsia (15–20 L/day)
  • Hypervolemic — renal failure, heart failure, liver failure, nephrotic syndrome
physiology · background · low-yield
Mechanism
  • Hypothyroidism mechanism — ↓ cardiac output → ADH release → ↓ urine → water retention
Background
  • Named SIADH causes by category — CNS (infection, stroke/tumour, trauma), pulmonary (TB, pneumonia), cancers (lung, pancreatic), drugs (SSRIs, TCAs)
3

Hypokalaemia

C/P
  • Muscle — weakness; paralysis if severe
  • Cardiac — arrhythmias
  • Renal — nephrogenic DI (K required for ADH effect on tubule)
Inves
  • Serum K — confirm hypokalaemia
  • ECG — flat T wave, prominent U wave
  • Serum Mg — often co-depleted; refractory K unless Mg replaced
  • Aldosterone / renin — for Conn's, secondary hyperaldosteronism screen
  • ECG — flat T wave, prominent U wave, ST depression, PR prolongation
Mng
  • Oral K supplementation — mild/moderate deficit with normal ECG
  • IV KCl — severe hypokalaemia, ECG changes, or unable to take orally; via central line if concentrated
  • Correct Mg — hypomagnesaemia perpetuates renal K wasting
  • Treat cause — stop offending diuretic, treat Conn's, replace GI losses
  • Avoid dextrose-containing IV fluids — use isotonic 0.9% saline as diluent; dextrose triggers insulin release → drives K into cells → worsens hypokalaemia
Special
  • Classic ECG signature — flat T + prominent U wave (opposite of hyperkalaemia's peaked T)
  • Causes — GI loss (vomiting, diarrhoea); transcellular shift into cells (insulin, β-agonists, alkalosis); renal loss (loop/thiazide diuretics, mineralocorticoid excess, tubular defects)
  • Tubular-defect causes — Bartter (Na-K-2Cl defect, ascending loop of Henle, mimics loop diuretic), Gitelman (Na-Cl defect, DCT, mimics thiazide), liquorice
physiology · background · low-yield
Other
  • Numeric severity cut-off — oral replacement if serum K > 2.5 mEq/L (no ECG changes); IV if < 2.5 mEq/L or symptomatic
Mechanism
  • Renal tubular causes — Bartter (Na-K-2Cl cotransporter defect, ascending loop of Henle, mimics a loop diuretic), Gitelman (Na-Cl cotransporter defect, distal tubule, mimics a thiazide), and liquorice
4

Hyperkalaemia

C/P
  • Muscle — weakness
  • Cardiac — abnormal conduction / heart block
Inves
  • Serum K — confirm; rule out haemolysed sample
  • ECG — peaked T wave
  • Renal function (urea/Cr) — CKD/AKI is dominant cause
  • Blood gas — associated metabolic acidosis
  • Aldosterone/cortisol — screen Addison's if hyponatraemic + hypotensive
  • Full ECG progression — peaked T → widening QRS → PR prolongation → low-amplitude P wave
  • ECG — peaked T wave, widening of QRS, PR prolongation, low-amplitude (flattened) P wave
Mng
  • Calcium gluconate IV — first line if ECG changes; membrane stabilisation, doesn't lower K
  • Insulin + dextrose — shifts K into cells via Na-K pump; dextrose prevents hypoglycaemia
  • Sodium bicarbonate — alkalosis drives K into cells in exchange with H+
  • Beta-2 agonist (nebulised salbutamol) — activates Na-K pump
  • Loop diuretics — increase urinary K excretion
  • Cation exchange resin — absorbs K from GIT → excreted in stool
  • Dialysis — last line if refractory; also for AEIOU indications in AKI
Special
  • Classic ECG signature — peaked T wave, then QRS widening (opposite of hypokalaemia's flat T + U)
  • Extracellular shift causes — cell lysis (rhabdo, tumour lysis), acidosis, insulin deficiency, beta blockers, digoxin
  • Decreased-excretion causes — drugs (K-sparing diuretics, ACE-i, ARBs → ↓aldosterone), decreased adrenal activity (Addison's), renal failure
physiology · background · low-yield
Mechanism
  • Hyperosmolarity — additional trigger of extracellular K shift (alongside cell lysis, acidosis, blocked shift-in)

Nephritic Syndromes

6 entries
5

Acute Post-Streptococcal GN (PIGN)

C/P
  • Acute nephritic syndrome — oliguria, haematuria, hypertension, mild proteinuria, mild oedema
  • 1–4 weeks after Group A β-haemolytic strep pharyngitis or skin infection
  • Typically childhood onset
Inves
  • ASOT (Anti-streptolysin O titre) — confirms recent strep infection
  • Complement — ↓ C3, normal C4 (alternative pathway activation)
  • Urinalysis — haematuria, RBC casts, mild proteinuria (<3 g/day)
  • Throat/skin swab — confirm ongoing infection if present
  • Renal biopsy — reserved for atypical course; shows enlarged hypercellular glomeruli, PMN infiltrate, sub-epithelial "humps" on EM
Mng
  • General supportive — fluid/salt restriction, antihypertensives for BP control
  • Antibiotics — only if ongoing strep infection (penicillin)
  • Self-limiting — full renal recovery expected in children
Special
  • Sub-epithelial "humps" on EM — pathognomonic deposit location
  • Only 1–2% progress to CKD (vs 30–50% for IgAN)
physiology · background · low-yield
Other
  • IF/EM deposits — granular IgG, IgM and C3 within the basement-membrane zone ± mesangial matrix
6

IgA Nephropathy (Berger's Disease)

C/P
  • Recurrent microscopic or gross haematuria — most common cause worldwide
  • Synpharyngitic — haematuria 1–2 days after URTI or GI infection (concurrent, not post)
  • Children and young adults (2nd/3rd decade)
  • Association with coeliac disease (mucosal disorder overlap)
Inves
  • Urinalysis — microscopic/gross haematuria with RBC casts
  • Serum IgA — elevated in 50% of cases (not sensitive enough alone)
  • Complement — normal C3, normal C4 (distinguishes from PIGN)
  • Renal biopsy — mesangial hypercellularity; IF: mesangial IgA deposits + C3; EM shows mesangial electron-dense deposits
Mng
  • Supportive — ACE-i / ARB if proteinuria to slow progression
  • Immunosuppressives — reserved for specific situations (rapidly progressive, high-risk features)
  • Treat ongoing infection with antibiotics
Special
  • Synpharyngitic haematuria (1–2 days post-infection) distinguishes from PIGN (1–4 weeks)
  • Mesangial IgA + C3 on IF — pathognomonic
  • 50% progress to CKD over time
physiology · background · low-yield
Epidemiology/Risk
  • Most common glomerular disease diagnosed by renal biopsy worldwide
Mechanism
  • Pathogenesis — some IgA is abnormally glycosylated, is deposited in the mesangium and activates the alternative complement pathway
7

Lupus Nephritis

C/P
  • Nephritic syndrome ± nephrotic features (varies by class)
  • Systemic SLE features — malar rash, photosensitivity, arthritis/arthralgia, serositis (pleuritis/pericarditis), seizures/psychosis, cytopenias, hair loss
  • Class IV (diffuse proliferative) — most severe, crescent formation
  • Class V (membranous) — nephrotic syndrome, mimics primary MN
Inves
  • Urinalysis — haematuria + proteinuria, RBC casts
  • ANA + Anti-dsDNA + Anti-Smith — serological triad; anti-dsDNA correlates with activity
  • Complement — ↓ C3, ↓ C4 (both consumed in classical pathway)
  • Renal biopsy — mandatory for classification (Classes I–VI); guides therapy
  • EM deposit location — Classes III/IV subendothelial, Class V subepithelial, Classes I–V mesangial
Mng
  • Immunosuppressive drugs — induction + maintenance dictated by class
  • Mycophenolate mofetil — induction and maintenance in proliferative classes
  • Cyclophosphamide — alternative induction agent in severe disease
  • Azathioprine — maintenance agent
  • Outcome variable — depends on severity and treatment response
Special
  • 6 histological classes (I minimal mesangial → VI advanced sclerosis)
  • Class IV distinguishing — diffuse lupus nephritis with crescent formation
  • Class V distinguishing — thickened GBM on silver stain (looks like membranous)
8

Goodpasture's Syndrome (Anti-GBM Disease)

C/P
  • Pulmonary-renal syndrome — haemoptysis + haematuria
  • Renal — nephritic syndrome or RPGN with severe oliguria
  • Pulmonary — pulmonary haemorrhage, haemoptysis
  • Triggers — smoking, organic solvents/hydrocarbons, cocaine inhalation, metal dust, viral infection (influenza, COVID-19)
Inves
  • Anti-GBM antibodies — diagnostic (target α3 chain of type IV collagen)
  • Urinalysis — haematuria, RBC casts, proteinuria
  • Renal biopsy — linear IgG deposits on IF along GBM; crescent formation on light microscopy
  • CXR — pulmonary infiltrates from alveolar haemorrhage
Mng
  • Plasma exchange (plasmapheresis) — emergency to remove circulating anti-GBM antibodies and save the kidney
  • Corticosteroids — suppress immune response
  • Cyclophosphamide — suppress ongoing antibody production
  • Rituximab — alternative B-cell depletion
  • Renal function often rapidly and irretrievably lost — treat urgently
Special
  • Linear IgG deposits on IF — pathognomonic (vs granular of PIGN, mesangial IgA of Berger's)
  • Alveolar BM only vulnerable after prior lung injury (smoking, infection) opens capillary permeability
physiology · background · low-yield
Background
  • Terminology — Goodpasture syndrome = diffuse pulmonary haemorrhage + acute/RPGN (clinical entity); Goodpasture disease = GN ± pulmonary haemorrhage with circulating anti-GBM antibodies
9

Rapidly Progressive (Crescentic) GN

C/P
  • Rapid, progressive loss of renal function with severe oliguria — death from renal failure in weeks–months untreated
  • Onset resembles nephritic syndrome but with more oliguria and azotaemia
  • 90% require dialysis or transplantation
Inves
  • Urinalysis — haematuria, RBC casts, proteinuria
  • Rapid rise in serum creatinine over weeks
  • Immune profile — anti-GBM, ANCA, ANA/anti-dsDNA to classify type
  • Renal biopsy — urgent, definitive; shows crescents (parietal epithelial proliferation + fibrin + mononuclear cells) → sclerose over time; EM shows GBM rupture
  • Gross — enlarged, pale kidney with petechiae
Mng
  • Aggressive immunosuppression — high-dose corticosteroids + cyclophosphamide
  • Plasma exchange — for Type I (anti-GBM) and severe ANCA-associated Type III
  • Rituximab — B-cell depletion alternative
  • Renal replacement therapy — most patients ultimately require dialysis or transplant
Special
  • Crescent formation — fibrin leakage from ruptured GBM triggers parietal epithelial proliferation into Bowman's space
  • Three IF types — I (linear/anti-GBM), II (granular/immune complex), III (pauci-immune/ANCA — Wegener's granulomatosis, PAN)
  • Type II (immune-complex) causes — idiopathic, SLE, post-infective (completes the classification: I anti-GBM/Goodpasture, II immune-complex, III pauci-immune/ANCA)
10

Alport Syndrome

C/P
  • Nephritic syndrome + recurrent macroscopic haematuria
  • Alport triad — nephritis + sensorineural deafness + ocular abnormalities
  • X-linked hereditary — males affected more severely
Inves
  • Urinalysis — persistent haematuria, proteinuria
  • Audiometry — confirm sensorineural hearing loss
  • Slit-lamp — anterior lenticonus, retinal flecks
  • Genetic testing — definitive diagnosis (type IV collagen gene mutation)
  • Renal biopsy — EM shows irregular splitting / "wavy" GBM appearance (basketweave)
  • Family screening — screen relatives for haematuria
Mng
  • No specific disease-modifying treatment
  • ACE-i / ARB — slow progression of proteinuria
  • Hearing aids; renal transplantation for ESRD
Special
  • Type IV collagen mutation — affects GBM, cochlea, eye
  • Wavy / basketweave GBM on EM — pathognomonic
  • Almost all cases progress to CKD

Nephrotic Syndromes

4 entries
11

Minimal Change Disease (MCD)

C/P
  • Nephrotic syndrome — massive proteinuria, generalised oedema, hypoalbuminaemia, hyperlipidaemia, lipiduria
  • Most common cause of nephrotic syndrome in children
  • Preceding events — respiratory tract infection, immunisation, atopy
  • Secondary adult triggers — Hodgkin's disease, NSAIDs
Inves
  • Urinalysis — heavy proteinuria (>3.5 g/day), lipiduria
  • Serum — hypoalbuminaemia, hyperlipidaemia
  • Renal biopsy — light microscopy normal, IF no deposits; EM: diffuse effacement of podocyte foot processes (only visible finding)
  • Screen for secondary cause — CXR/lymphoma workup, drug history (NSAIDs)
Mng
  • Corticosteroids — first line, usually dramatically effective at inducing remission
  • Cyclosporine or tacrolimus — steroid-resistant or frequent relapsers
  • Treat cause — stop NSAID, treat Hodgkin's
  • Relapse common; overall good prognosis
Special
  • Lipoid nephrosis — lipid-laden PCT epithelial cells; only visible on histology
  • EM podocyte effacement — pathognomonic (glomerulus otherwise normal)
  • Steroid-responsive → distinguishes from FSGS
physiology · background · low-yield
Mechanism
  • Pathogenesis — immune dysfunction releasing a circulating cytokine-like (T-cell) permeability factor that acts on visceral epithelial cells/podocytes
12

Focal Segmental Glomerulosclerosis (FSGS)

C/P
  • Nephrotic syndrome — non-selective proteinuria, generalised oedema
  • Often steroid-resistant in children
  • Common associations — haematuria, ↓GFR, hypertension
  • Secondary triggers — HIV, heroin, obesity, pamidronate, interferon
Inves
  • Urinalysis — heavy non-selective proteinuria, haematuria
  • HIV test, drug history, BMI — screen secondary causes
  • Renal biopsy — segmental sclerosis starting at juxtamedullary glomeruli; EM: diffuse podocyte effacement + denuded GBM + detached epithelial cells; IF: IgM + C3 within hyaline masses
  • Genetic testing — hereditary form (TRPC6 mutation)
Mng
  • Corticosteroids — first line for primary, but often steroid-resistant
  • Cyclosporine / tacrolimus — steroid-resistant cases
  • Treat the cause — antiretrovirals for HIV, weight loss, stop heroin/pamidronate
  • ACE-i / ARB — slow progression
Special
  • Starts at juxtamedullary zone → spreads outward — deep biopsy required or lesion missed
  • Almost all cases progress to CKD (50% at 10 y, 20% within 2 y rapid-progressors)
  • Hereditary form — TRPC6 gene mutation
physiology · background · low-yield
Mechanism
  • Adaptive FSGS — glomerular ablation/nephron loss → compensatory hyperfiltration + capillary hypertension in surviving glomeruli → vicious circle of glomerulosclerosis
13

Membranous Nephropathy (MN)

C/P
  • Nephrotic syndrome — major cause in adults
  • Older middle-aged adults (50–60 y), men > women
  • Primary autoimmune; secondary to systemic disease
  • Secondary triggers — malignancy, HBV, HCV, HIV, SLE, NSAIDs
  • High risk of thromboembolic events (loss of antithrombin III in urine)
Inves
  • Urinalysis — heavy proteinuria
  • Anti-PLA2R antibodies — diagnostic for primary MN (target podocyte antigen)
  • Screen for secondary cause — malignancy workup (age-appropriate cancer screening), HBV/HCV serology, HIV, ANA
  • Renal biopsy — thickened GBM on light microscopy; EM: irregular sub-epithelial deposits with loss of epithelial foot processes; IF: granular IgG + C3
Mng
  • Immunosuppressive drugs — primary MN
  • Treat cause — for secondary MN (antivirals for HBV/HCV, cancer treatment)
  • ACE-i / ARB — reduce proteinuria
  • 75% remit; 25% progress to CKD
Special
  • Anti-PLA2R — specific marker for primary MN (podocyte phospholipase A2 receptor)
  • Sub-epithelial deposits — mimicked by Lupus Class V and post-strep GN
physiology · background · low-yield
Mechanism
  • Primary MN autoantibody targets an antigen on the basal surface of podocytes, cross-reacting with proximal-tubule brush-border antigens → diffuse granular sub-epithelial deposits
Epidemiology/Risk
  • ~80% of membranous nephropathy is primary (in-situ anti-PLA2R); the remaining ~20% is secondary (malignancy, HBV/HCV/HIV, SLE, NSAIDs)
Mechanism
  • Immune-deposit location follows molecular charge — neutral molecules → mesangial deposits, cationic → sub-epithelial, anionic → sub-endothelial or no deposits; a large circulating immune complex that cannot cross the GBM causes no nephritis
14

Membranoproliferative GN (MPGN)

C/P
  • Mixed nephrotic + nephritic features
  • Secondary triggers — HCV, HBV, SLE, plasma cell dyscrasias
  • Hereditary form — alternative complement pathway dysregulation
Inves
  • Urinalysis — mixed proteinuria + haematuria
  • Complement — ↓ C3, normal C4 (alternative pathway consumption)
  • HCV/HBV serology, immunoglobulins, autoantibodies — secondary screen
  • Renal biopsy — Type 1: sub-endothelial deposits; Type 2 (dense deposit disease): intramembranous deposits; Type 3: sub-endothelial + sub-epithelial deposits
  • Genetic testing — hereditary complement dysregulation forms
  • Complement pattern differs by type — Types 1 & 3 activate the classical pathway → ↓ C3 and ↓ C4; Type 2 activates the alternative pathway → ↓ C3, normal C4
Mng
  • Treat cause — antivirals for HCV, treat myeloma
  • Immunosuppression — corticosteroids, cyclophosphamide, mycophenolate mofetil
  • ACE-i / ARB — reduce proteinuria
  • 50% progress to CKD
Special
  • Type 2 = dense deposit disease with intramembranous "ribbon" deposits
  • Alternative complement pathway over-activation drives hereditary forms
physiology · background · low-yield
Mechanism
  • Primary MPGN — circulating immune-complex deposition drives the mesangiocapillary proliferation

End-Stage Glomerulonephritis

1 entry
15

Chronic Glomerulonephritis

C/P
  • End-stage of many glomerular lesions
  • Insidious course; progressive proteinuria, hypertension, azotaemia
  • Transient episodes of nephrotic or nephritic features
  • As glomeruli obliterate → proteinuria falls, hypertension dominates
Inves
  • Serum urea + creatinine — established renal failure
  • Ultrasound — bilateral symmetrically contracted small kidneys with granular surface
  • Renal biopsy — rarely helpful at end stage (primary cause unrecognisable); shows hyalinised glomeruli, tubular atrophy, interstitial fibrosis + lymphocytic infiltrate, arteriolar sclerosis
Mng
  • Manage as CKD — BP control (ACE-i/ARB), renoprotection, avoid nephrotoxins
  • Prepare for RRT — dialysis or transplantation once GFR < 15
Special
  • Bilateral symmetrical contracted kidneys with diffuse granular surface — gross hallmark
  • "Ghost" glomeruli — totally acellular hyalinised on microscopy at late stage
  • Precursor progression rates — RPGN 90%, FSGS 50–80%, MN 50%, MPGN 50%, IgAN 30–50%, PIGN 1–2%
  • Cut section — thin cortex with increased peri-pelvic fat (gross hallmark of the contracted end-stage kidney)
physiology · background · low-yield
Background
  • Microscopy — early stage still shows evidence of the primary lesion, only later becoming totally acellular/hyalinised (ghost) glomeruli

Cystic Kidney Disease

1 entry
16

Autosomal Dominant Polycystic Kidney Disease (ADPKD)

C/P
  • Renal — hypertension, recurrent UTIs, abdominal pain, renal stones, haematuria (from stones or ruptured cyst), progression to CKD
  • Extra-renal cysts — liver (70%, most common extra-renal), pancreas, spleen; rare thyroid/oesophagus/ovary
  • Berry aneurysms (8%) — risk of subarachnoid haemorrhage on rupture
  • Cardiac/aortic — MVP, MR/TR, aortic root dilation, aortic dissection
  • Hepatomegaly — palpable enlarged liver from massive hepatic cysts
Inves
  • Ultrasound — screening investigation for relatives; age-based cyst-count diagnostic criteria in family-history-positive patients
  • CT abdomen — enlarged kidneys with innumerable cysts (mm to cm), little remaining parenchyma, associated liver cysts
  • MR angiography of brain — screen for berry aneurysms in high-risk patients / family history of SAH
  • Genetic testing — confirm PKD1 vs PKD2 for prognosis
Mng
  • Tolvaptan — vasopressin V2 receptor antagonist; slows cyst growth (NICE: CKD stage 2 or 3 at start, rapidly progressing disease, discount agreed via patient access scheme)
  • BP control — ACE-i / ARB first line
  • Manage complications — UTIs, stones, pain
  • Screen and manage berry aneurysms if positive family history
  • Prepare for RRT — dialysis or transplant at ESRD
Special
  • PKD1 (85%, chromosome 16) — earlier ESRD; PKD2 (15%, chromosome 4) — later ESRD
  • Cysts arise from tubules, not glomeruli
  • Pathogenesis — polycystin mutation → ↓intracellular Ca → disinhibited adenylyl cyclase → ↑cAMP → AVP/V2 amplification → cell proliferation + fluid secretion
physiology · background · low-yield
Epidemiology/Risk
  • Most common inherited cause of kidney disease
  • Prevalence 1 in 1,000 in Caucasians
Mechanism
  • PKD1 encodes polycystin-1; PKD2 encodes polycystin-2

Interstitial & Toxic Nephropathies

6 entries
17

Drug-Induced Acute Interstitial Nephritis (AIN)

C/P
  • Classic triad (minority only) — fever + arthralgia + skin rash
  • Often asymptomatic — AKI found incidentally on bloods
  • Oliguric or non-oliguric AKI
  • Tubular defects — aminoaciduria, glycosuria, renal tubular acidosis
  • Culprits — NSAIDs, PPIs, penicillins, rifampicin, cephalosporins, ciprofloxacin, erythromycin, sulphonamides, furosemide/thiazides, allopurinol, phenytoin, carbamazepine, valproate, cimetidine
  • Non-drug causes — infection (acute pyelonephritis with neutrophilic infiltrate; CMV/BK-polyoma/HSV in renal grafts), autoimmune (Sjögren, SLE, sarcoidosis), and TINU (tubulointerstitial nephritis with uveitis) — idiopathic ~5% of cases
Inves
  • Bloods — eosinophilia; AKI biochemistry
  • Urine — eosinophiluria, mild proteinuria, haematuria, pus cells; WBC casts
  • Renal ultrasound — normal kidney size (rules out CKD/obstruction)
  • Renal biopsy — definitive; interstitial mononuclear + eosinophilic infiltrate, sparing of glomeruli, variable tubular necrosis; NSAID-induced AIN may show concurrent minimal change lesion
Mng
  • Stop the offending drug — cornerstone of management
  • High-dose prednisolone 60 mg daily — reduces risk of dialysis-requiring AKI and shortens recovery time
  • Most recover; residual interstitial fibrosis and CKD possible
Special
  • Eosinophilic infiltrate with glomerular sparing — pathognomonic biopsy pattern
  • NSAID-induced AIN uniquely can present with concurrent minimal change lesion → nephrotic syndrome
physiology · background · low-yield
Epidemiology/Risk
  • Accounts for 10–15% of kidney diseases; by cause: drugs 70% (most common), infection 15%, idiopathic 8%, systemic inflammatory ~2%
Mechanism
  • Pathogenesis — injury to renal cells → new local antigen expression → cytokines from infiltrating macrophages/lymphocytes and resident cells (proximal tubule, endothelial, interstitial, fibroblasts) → interstitial inflammatory infiltrate → acute or chronic nephritis
Other
  • Histology — tubulitis (inflammatory cells within the tubular wall) with neutrophils in peritubular capillaries alongside the eosinophil-rich infiltrate
18

Chronic Tubulointerstitial Nephritis

C/P
  • Insidious onset
  • Polyuria + nocturia — from concentrating defect
  • Hypertension, uraemia
  • Slight proteinuria (<1 g/day) — glomeruli spared
  • Causes — analgesics, ciclosporin, 5-ASA, heavy metals (cadmium, lead, titanium), radiation, diabetes, sickle cell, SLE/vasculitis, sarcoidosis, IgG4 disease, hyperuricaemia, nephrocalcinosis, hyperoxaluria, HIV, EBV, hypertension, Balkan nephropathy, herbal nephropathy, Alport
Inves
  • Renal function + electrolytes — slowly rising Cr
  • Urinalysis — mild proteinuria <1 g/day, no active sediment
  • Occupational + drug history — screen for heavy metals, analgesics
  • Renal biopsy — chronic mononuclear infiltrate in interstitium, tubular atrophy, interstitial oedema + fibrosis
Mng
  • Remove offending exposure — stop analgesics, chelation for heavy metals, treat underlying disease
  • Renoprotection — BP control, avoid further nephrotoxins
  • Manage as CKD — RRT preparation if ESRD
Special
  • Sub-nephrotic proteinuria distinguishes from glomerular disease
  • Sarcoidosis form — granulomatous tubulointerstitial nephritis
physiology · background · low-yield
Mechanism
  • Loss of tubular resorptive capacity → glycosuria with normal blood glucose, alkaline urine, and low serum phosphate + bicarbonate (pattern depends on the tubular site affected)
19

Papillary Necrosis (Analgesic Nephropathy)

C/P
  • Microscopic or overt haematuria; occasional sterile pyuria
  • Ureteric colic + acute ureteric obstruction from sloughed papilla
  • Chronic analgesic use — historically phenacetin, now NSAIDs (± acetaminophen, ± caffeine)
  • Systemic associations — sickle cell, diabetes
Inves
  • Urinalysis — haematuria, sterile pyuria
  • IVP / CT urography — bilateral ring sign (sloughed papilla), clubbed calyces, spurs, hooks; no cortical loss
  • Drug + occupational history — chronic NSAID use
  • Screen for underlying disease — sickle cell, diabetes
Mng
  • Stop offending analgesic — cornerstone
  • Relieve ureteric obstruction if present
  • Manage sickle cell / diabetes; renoprotection
Special
  • Ring sign + clubbed calyces — sloughed papillae on IVP
  • Always bilateral, no cortical loss — distinguishes from other renal shrinkage patterns
  • Ischaemic damage to papillae — sloughs into calyces and urine
20

Obstructive Uropathy

C/P
  • Causes — prostate disease, stones, neoplasm, retroperitoneal fibrosis
  • Modest proteinuria, hyperkalaemic renal tubular acidosis
  • Prostatic — hesitancy, frequency; palpable bladder + suprapubic dullness
  • Chronic → CKD from tubulointerstitial disease
Inves
  • Ultrasound of kidneys and bladder — mandatory in AKI to exclude obstruction (reversible once relieved)
  • IVP — bilateral hydronephrosis + hydroureter + irregular trabeculated bladder wall (denotes outlet obstruction)
  • PSA + prostate examination if male
  • Urinalysis + culture — associated infection
Mng
  • Urethral catheter — immediate relief of bladder outlet obstruction
  • Nephrostomy / stent — upper tract obstruction
  • Treat cause — BPH, stones, tumour, retroperitoneal fibrosis
Special
  • Congenital VUR + chronic obstruction → secondary focal glomerulosclerosis with nephrotic syndrome in adult life
  • Chronic recurrent UTI + obstruction → ammonium magnesium phosphate (struvite) stones
21

Lead Nephropathy

C/P
  • High-risk occupations — welders, smelters, battery workers, painters/restorers of old buildings (poorly ventilated environments)
  • Hypertension almost always present — misdiagnosed as "hypertensive kidney disease"
  • Gout — common ("saturnine gout")
  • Disproportionately worse hyperuricaemia than other kidney diseases
Inves
  • Serum uric acid — disproportionately elevated
  • Occupational history + blood lead level — confirms exposure
  • Bone lead measurement — for chronic exposure
Mng
  • Remove exposure — first line
  • Chelation therapy — for high lead burden
  • Treat gout — colchicine, allopurinol
  • BP control
Special
  • Unique lead effect on urate metabolism → saturnine gout
22

Hypercalcaemic Nephropathy

C/P
  • Most common cause of metabolic nephropathy
  • Polyuria + concentrating defect (nephrogenic DI)
  • Causes — primary hyperparathyroidism, sarcoidosis, multiple myeloma, bone metastases, vitamin D intoxication
Inves
  • Serum Ca + PTH + PO4 + Vit D — localise cause (↑PTH primary HPT; ↓PTH malignancy/Vit D)
  • Urine osmolality — concentrating defect
  • Ultrasound / X-ray — nephrocalcinosis, renal stones
  • Cause-specific workup — SPEP for myeloma, chest imaging for sarcoid
Mng
  • Correct hypercalcaemia — IV saline + loop diuretics; bisphosphonates for malignancy
  • Treat cause — parathyroidectomy, corticosteroids for sarcoid, treat myeloma
Special
  • Ca deposits confined to distal tubular structures → impaired concentrating ability → polyuria (nephrogenic DI)

Acute Renal Injury

6 entries
23

Acute Kidney Injury (AKI)

C/P
  • Abrupt deterioration in renal function over hours–days, usually reversible
  • Acute symptoms — dyspnoea, N/V, diarrhoea
  • Common — 1 in 5 hospitalised adults, 1 in 3 hospitalised children; ~5% UK community admissions; sepsis (25%) or septic shock (50%)
  • 3 anatomical categories — pre-renal (hypoperfusion), renal parenchymal, post-renal (obstruction)
  • Pre-renal causes — hypovolaemia (dehydration, haemorrhage), hypotension without hypovolaemia (cirrhosis, septic shock), low cardiac output (cardiac failure, cardiogenic shock)
  • Intrinsic (renal parenchymal) — 4 subtypes: ATN (80–90%), glomerular (acute RPGN), acute tubulointerstitial, vascular (vasculitis, accelerated hypertension, cholesterol embolism, HUS)
  • Post-renal — prostate disease (men) or bilateral ureteric obstruction (stones/tumours); hesitancy + frequency; palpable bladder + suprapubic dullness on exam
  • Assess volume status — hypovolaemia signs: low BP, rapid pulse, sunken eyes, collapsed neck veins
Inves
  • Serum urea + creatinine + eGFR — stage per RIFLE/AKIN/KDIGO
  • Blood urea to creatinine ratio > 20:1 (urea:creatinine >40:1) — suggests pre-renal
  • Urine chemistry — FENa <1%, urine Na <10, urine osm >500 in pre-renal; opposite in intrinsic
  • Urinalysis — RBC casts (glomerulonephritis), free Hb/myoglobin, pigmenturia
  • Early biomarkers — KIM-1, NGAL rise within hours
  • Serum chemistry — U&E, Ca, PO4, albumin, ALP, urate; CBC, coagulation, blood cultures, nephrotoxic drug levels; immune profile if GN suspected
  • Ultrasound of abdomen + pelvis — mandatory to exclude obstruction; check bladder
  • Renal biopsy — indicated if unexplained urine abnormalities (proteinuria/haematuria), persistent ATN >4 weeks, unclear aetiology, suspected systemic disease
  • Acute vs chronic — kidneys normal size on US in AKI vs small in CKD (except diabetes, where CKD kidneys stay normal/large); previous creatinine normal; anaemia, high PTH, hyperphosphataemia and hypocalcaemia less common than in CKD
Mng
  • Fluid balance — daily weights, lying/standing BP, intake/output; withhold nephrotoxins
  • Pre-renal — fluid challenge of 250 mL crystalloid; Plasmalyte or Ringer's lactate preferred over 0.9% saline (avoid hyperchloraemic acidosis)
  • Post-renal — urethral catheter + upper tract imaging; nephrostomy for upper tract obstruction
  • Intrinsic ATN — DO NOT give fluid once established; supportive
  • Treat hyperkalaemia, acidosis, pulmonary oedema, sepsis
  • Adjust drug doses daily; particular care with anticoagulants; salt + K restriction
  • RRT indications (all 5) — symptomatic uraemia (encephalopathy/pericarditis/tamponade), refractory hyperkalaemia, refractory pulmonary oedema, severe acidosis, drug removal (gentamicin, lithium, severe aspirin overdose)
Special
  • Uncomplicated AKI mortality <5–10%; ITU + multi-organ failure 50–70%; sepsis-associated AKI much worse prognosis
  • Autoregulation defence — prostaglandins on afferent arteriole (blocked by NSAIDs); angiotensin II on efferent arteriole (blocked by ACE-i)
physiology · background · low-yield
Epidemiology/Risk
  • In half of community-acquired AKI cases, the AKI is superimposed on pre-existing CKD
24

Acute Tubular Necrosis (ATN)

C/P
  • Final common pathway for many insults — accounts for 80–90% of intrinsic AKI
  • Ischaemic ATN — trauma, septicaemia, acute pancreatitis, hypotension/shock
  • Nephrotoxic ATN — poisons, drugs (aminoglycosides, contrast agents), organic solvents, myoglobin (rhabdo)
  • Four classical phases — onset (36 h) → oliguric (few days–3 weeks, marked oliguria + uraemia) → diuretic (polyuria >3 L/day) → recovery (weeks); usually partial residual impairment
Inves
  • Urea/creatinine rising over days
  • Urine — muddy brown granular casts, renal tubular epithelial cell casts
  • Urine Na > 20, FENa >1%, urine osm <350 — distinguishes from pre-renal
  • Ultrasound — normal or enlarged kidneys (rule out post-renal)
  • Renal biopsy if persistent >4 weeks or unclear cause
Mng
  • DO NOT give fluid in established ATN — supportive only
  • Withhold nephrotoxins; adjust doses of renally cleared drugs
  • Treat hyperkalaemia, acidosis, fluid overload, sepsis
  • RRT — for AEIOU indications: refractory Acidosis, Electrolytes (K >6.5), Intoxications, Overload, Uraemic complications
  • Recovery over 7–21 days; sepsis delays recovery
Special
  • Nephrotoxic ATN — spares basement membrane, targets whole PCT → good regeneration
  • Ischaemic ATN — focal rupture of tubular basement membrane → incomplete regeneration in those areas
  • Gross — enlarged kidney, pale necrotic cortex, congested medulla
  • Two oliguria mechanisms — (1) tubular damage → renin-angiotensin → afferent VC → ↓GFR; (2) debris blocks lumen → ↑intratubular pressure → fluid leak to interstitium → collapsed tubules
  • Non-oliguric AKI usually reflects a less severe renal insult (better prognosis); oliguria is the common early finding
physiology · background · low-yield
Mechanism
  • Three core pathogenic mechanisms — intrarenal microvascular vasoconstriction (hypoxia), endothelial + vascular smooth-muscle structural damage, tubular cell injury; tubular epithelium is most vulnerable to ischaemia due to its high metabolic rate
  • Interstitium is oedematous + hyperaemic with an infiltrate of polymorphs, lymphocytes and plasma cells (in both ischaemic + nephrotoxic ATN)
25

Rhabdomyolysis

C/P
  • Skeletal muscle injury releases myoglobin → nephrotoxic ATN ("crush syndrome")
  • Causes — trauma, compartment syndrome, excessive exertion (marathon runners), status epilepticus
  • Muscle toxins — statins, malaria/antimalarials, snake/insect venom
  • Dark brown / tea-coloured urine + oliguria + AKI
Inves
  • Urine dipstick — positive for blood, but no RBCs on microscopy (myoglobin cross-reactivity)
  • Elevated markers — K↑, PO4↑, CPK↑↑ (creatine phosphokinase)
  • Serum myoglobin
  • Renal function — rising BUN/creatinine consistent with ATN
  • Assess for compartment syndrome — surgical review
Mng
  • Aggressive IV fluid resuscitation — crystalloids to maintain urine output and flush myoglobin
  • Treat hyperkalaemia — insulin/dextrose, calcium gluconate for ECG changes
  • Fasciotomy — if compartment syndrome
  • Haemodialysis if severe AKI or refractory hyperkalaemia
  • Tubular epithelium regenerates with supportive care
Special
  • Urine dipstick positive for blood but no RBCs on microscopy — pathognomonic for myoglobin/haemoglobin
  • Classic AKI arc — oliguric maintenance phase → recovery phase polyuria (>3 L/day) as tubules recover before concentrating ability
26

Tumour Lysis / Acute Hyperuricaemic Nephropathy

C/P
  • Complication of first cytotoxic/steroid treatment of lymphoproliferative tumours
  • Massive tumour cell lysis releases intracellular contents — URIC ACID, K, PO4
  • Uric acid crystal deposition in collecting ducts, pelvis, ureters → intrarenal + extrarenal obstruction → AKI
Inves
  • Serum uric acid, K, PO4, Ca (may be low), LDH
  • Renal function — rising urea/creatinine
  • Ultrasound — may show extrarenal obstruction due to urate stones, or be unremarkable
Mng
  • Allopurinol — prior to and throughout cytotoxic/radiotherapy treatment (prophylaxis)
  • Aggressive IV fluids — maintain high urine output
  • Sodium bicarbonate — alkalinise urine to solubilise urate
  • Febuxostat — if allopurinol not tolerated + eGFR >30
  • Rasburicase — recombinant urate oxidase; converts urate to soluble allantoin
  • Dialysis — severely oliguric/anuric patients
Special
  • URIC ACID — highlighted release; primary cause of obstruction
27

Contrast Nephropathy

C/P
  • AKI 24–72 h after iodinated contrast administration
  • Risk factor — patients with impaired renal function at baseline
Inves
  • Baseline creatinine + rise post-contrast — confirms diagnosis
  • Screen for concomitant nephrotoxins
Mng
  • Prevention — IV fluid pre- and post-contrast in high-risk patients; use minimum contrast volume
  • Withhold nephrotoxins around the study
  • Supportive management of AKI
Special
  • Two mechanisms — renal vasoconstriction + direct tubular toxicity
28

Hepatorenal Syndrome

C/P
  • Renal failure in a patient with liver cirrhosis + portal hypertension + ascites
  • Kidneys histologically normal — functional AKI
Inves
  • Diagnosis of exclusion — rule out pre-renal, structural, and intrinsic causes
  • Urine Na typically very low (functional pre-renal state)
  • LFTs + clotting — established chronic liver disease
  • Abdominal imaging — cirrhosis, ascites, portal hypertension features
Mng
  • Treat underlying liver disease
  • Supportive; profound renal vasoconstriction is functional, not structural
Special
  • Splanchnic vasodilation → reflex severe renal vasoconstriction; kidneys structurally intact

Vascular Renal Disease

4 entries
29

Renal Artery Stenosis (Atherosclerotic & Fibromuscular Dysplasia)

C/P
  • Unilateral small kidney + resistant hypertension → suggests renovascular disease
  • Atherosclerotic RAS — older heavy smoker with hypertension; ostial lesion
  • Fibromuscular dysplasia — typical age 35, often female; mid-to-distal artery
  • RAS = commonest cause of hypertension in mid-20s
Inves
  • Ultrasound — asymmetric kidney sizes (12 cm vs 9 cm on typical case)
  • Isotope renogram (DTPA — fewer hazards; MAG3) — assesses split function
  • Captopril renogram — ACE inhibitor drops GFR massively on the diseased side (loses efferent constriction dependency) → confirms renovascular hypertension
  • CT angiography — detailed anatomy; localise ostial vs distal lesion
  • Digital subtraction angiography — definitive + allows treatment; FMD shows classic "beaded" appearance
Mng
  • Medical — ACE-i / ARB with caution (monitor for AKI); statins for atherosclerosis; antihypertensives to target BP <130/80
  • Angioplasty ± stenting — for FMD (highly effective) and selected atherosclerotic cases
  • Smoking cessation + CV risk factor control for atherosclerotic disease
Special
  • Beaded appearance on angiography — FMD hallmark (mid-to-distal artery)
  • Must exclude before diagnosing essential hypertension in young or resistant hypertensives
physiology · background · low-yield
Mechanism
  • Atherosclerotic (senile) kidney — atheroma of the renal artery → infarction, ischaemic atrophy, fibrosis → contracted kidney with an irregular outer surface
  • Atherosclerotic (senile) kidney — atheroma of the renal artery → infarction, ischaemic atrophy, fibrosis → contracted kidney with an irregular outer surface
Other
  • Normal collective relative function on isotope renogram = 100% (both kidneys combined); DTPA carries fewer hazards than MAG3
30

Benign Nephrosclerosis

C/P
  • Slow, progressive renal impairment on background of chronic hypertension
  • Insidious course over years — bilateral symmetrical atrophy
Inves
  • Urinalysis — mild proteinuria
  • Ultrasound — bilateral symmetrical fine granular ("leather-like") surface; small kidneys
  • Renal biopsy — hyaline arteriolosclerosis (leaked plasma proteins + ↑matrix in vessel wall), fibrous intimal + medial thickening, luminal narrowing → tubular atrophy + interstitial fibrosis + focal global glomerulosclerosis; minimal inflammatory infiltrate
Mng
  • Manage as CKD — BP control (ACE-i/ARB first line), renoprotection, statin, avoid nephrotoxins
Special
  • "Leather-like" bilateral symmetrical granular surface — macroscopic hallmark
  • Fibroelastic hyperplasia — duplication of internal elastic lamina in interlobar/arcuate arteries
physiology · background · low-yield
Mechanism
  • Leather-like granular surface = subcapsular scars + sclerotic glomeruli + tubular atrophy alternating with preserved (raised, bulging) areas of parenchyma
31

Malignant Hypertension

C/P
  • BP > 200/120 mmHg; may arise de novo (arteritis, coagulopathy) or superimposed on longstanding benign HTN
  • Early symptoms from ↑ICP — headache, N/V, visual impairment
  • Full syndrome — papilloedema + encephalopathy + cardiovascular abnormalities + renal failure
  • Without treatment: 90% mortality within 1 year; with treatment: 75% 5-year survival
Inves
  • BP measurement — confirm >200/120
  • Fundoscopy — papilloedema, haemorrhages, exudates
  • Renal function — rapidly rising creatinine
  • Urinalysis — haematuria, proteinuria
  • Peripheral blood film — low Hb + low platelets → microangiopathic process
  • Renal biopsy — arteriolar fibrinoid necrosis + hyperplastic "onion-skin" arteriosclerosis; glomerular necrosis
Mng
  • ICU admission + IV antihypertensives — controlled BP reduction (avoid rapid drop)
  • Treat underlying cause if identified
Special
  • Flea-bitten kidney — petechial hemorrhages from ruptured arterioles / glomerular capillaries
  • Fibrinoid necrosis + onion-skin arteriosclerosis — microscopic pathognomonic pair (vs benign HTN's hyaline arteriolosclerosis)
  • PDGF released by trapped platelets → intimal cell proliferation → onion-skinning
32

Haemolytic Uraemic Syndrome (HUS)

C/P
  • Thrombotic microangiopathy of renal small vessels
  • Peripheral features — low Hb + low platelets; other vascular beds may show signs
  • Genetic predisposition ± exogenous trigger
Inves
  • CBC — anaemia, thrombocytopenia
  • LDH↑, haptoglobin↓ — haemolysis markers
  • Renal function — rising creatinine
  • Stool culture — shiga-toxin-producing E. coli in typical/diarrhoea-associated form
  • Complement studies — screen atypical HUS (complement regulatory protein defects)
  • Renal biopsy — thrombotic microangiopathy; affects some renal vessels more than others
Mng
  • Supportive — fluid management, transfusion, dialysis for AKI
  • Treat the underlying trigger (exogenous toxin or complement defect)
Special
  • Two mechanisms of endothelial injury — complement regulatory protein abnormalities; exogenous toxins (shiga)
physiology · background · low-yield
Mechanism
  • Thrombotic microangiopathy (TMA) — endothelial damage → coagulation activation + small-vessel occlusion → peripheral microangiopathic picture (low Hb, low platelets); shared by malignant hypertension, scleroderma, and HUS

Chronic Kidney Disease

1 entry
33

Chronic Kidney Disease (CKD)

C/P
  • Longstanding (>3 months) potentially progressive impairment
  • Early symptoms nonspecific; uraemic symptoms typically at eGFR < 10
  • Uraemic — anorexia/N/V, lethargy, poor concentration, pruritus, breathlessness (fluid overload/acidosis/anaemia), peripheral oedema
  • Physical signs — yellow complexion, pallor, brown-line pigmentation of nails, excoriations, bruising; Kussmaul respiration in acidosis; pericardial rub; peripheral neuropathy, restless legs; pitting oedema; dialysis/transplant access scars (Tenckhoff catheter, AV fistula, transplant scar)
  • Top causes — diabetes + hypertension; also glomerular, tubulointerstitial, vascular, obstructive, congenital
  • Anaemia of CKD — EPO deficiency + blood loss + haematinic deficiency + shortened RBC lifespan → LVH, MI, HF, ↑mortality
  • CKD-MBD — low Ca, high PTH, high PO4, low Vit D; osteitis fibrosa cystica, adynamic bone disease, vascular calcification
  • Cardiovascular disease is the major complication — sudden cardiac death, MI, cardiac failure, stroke, peripheral vascular disease; proteinuria adds further risk
  • Uraemic encephalopathy — asterixis, tremor, myoclonus, decreased seizure threshold, impaired cognition/anxiety/depression
Inves
  • Renal function — urea, creatinine, eGFR (KDIGO staging G1–G5)
  • Electrolytes/acid-base — Na, K, bicarbonate, ABG
  • Bone mineral — Ca, PO4, PTH; Vit D
  • Anaemia workup — iron, TIBC, TSAT, ferritin
  • Other — urate, lipids, HbA1c, ANA/anti-dsDNA if autoimmune suspected
  • Proteinuria — ACR (mg/mmol A1<3, A2 3–30, A3 >30) or 24 h urinary protein
  • Urinalysis — haematuria, pyuria
  • Ultrasound — gold standard imaging; normal size 9–12 cm; small + echogenic as CKD advances; except diabetics (normal/large)
Mng
  • Treat underlying cause — relieve obstruction, immunosuppression for GN/vasculitis, control accelerated HTN, correct critical renal artery stenosis
  • Renoprotection — ACE-i / ARB — first line if proteinuric, target proteinuria <0.3 g/24 h, add diuretic to prevent hyperkalaemia; add CCB (verapamil / diltiazem) as second line
  • BP targets — SBP 130 or <140 if tolerated (18–65); 130–139 if tolerated (65+); DBP 70–79 across ages
  • Statin for lipid lowering
  • Diabetic — HbA1c <7% (53 mmol/mol); SGLT2 inhibitor indicated
  • Dietary protein target 0.8 g/kg; smoking cessation (3× faster deterioration if smoking)
  • Avoid nephrotoxins (NSAIDs, aminoglycosides); dose-adjust renally cleared drugs; monitor K-sparing agents
  • Anaemia — Epoetin-α / darbepoetin-α (monitor for hypertension in first 6 months, ~30% side effect); iron — oral (ferrous sulfate, ferric citrate) if not on HD; IV iron (iron dextran, iron sucrose) if on HD; KDIGO iron trial: ferritin ≤500 ng/mL and TSAT ≤30%
  • CKD-MBD — phosphate binders (calcium acetate/carbonate with meals; sevelamer carbonate; aluminium binders with caution — bone disease + cognitive impairment); calcitriol / alfacalcidol; cinacalcet (calcimimetic) — tertiary hyperparathyroidism; goals: normal Ca/PO4, PTH 2–3× ULN on dialysis
  • Prepare for RRT at GFR < 15 — indications include fluid overload, severe HTN, uraemic symptoms, hyperkalaemia, acidosis (all refractory)
  • Prognosis correlates with BP control, proteinuria, interstitial scarring (not glomerular changes)
  • Gout (urate retained as GFR falls) — colchicine for acute attacks (avoid nephrotoxic NSAIDs); reduced-dose allopurinol or febuxostat for prevention
Special
  • Diabetic kidneys stay normal/large — exception to CKD size rule
  • β₂-microglobulin amyloidosis → carpal tunnel syndrome in long-term dialysis
  • Adynamic bone disease — if PTH suppressed >3-fold; hypercalcaemia risk
  • Hyperparathyroid bone disease (osteitis fibrosa cystica) — digital subperiosteal erosions; rugger-jersey spine (sclerotic bands at vertebral body endplates)
  • Vascular calcification — driven by calcium-phosphate product > 55, hyperparathyroidism, uraemia, inflammation; detected on X-ray of lumbar spine/abdomen
  • Insulin requirements fall as CKD progresses (↓ renal insulin clearance + ↓ renal gluconeogenesis) → hypoglycaemia risk if diet unchanged; also insulin resistance
physiology · background · low-yield
Mechanism
  • Progression is etiology-independent once ~half of nephrons are lost — ↓ nephron number → adaptive hyperfiltration + RAAS activation → ↑ glomerular permeability → proteinuria → nephrotoxic inflammation → tubulointerstitial fibrosis + 2° FSGS; Ang II ↑ TGF-β (fibrogenic) → collagen synthesis + epithelial-to-myofibroblast transdifferentiation (ACE-i breaks the cycle)
  • Anaemia mechanism — hypoxia-inducible factor (HIF) degraded in normoxia, in hypoxia drives EPO gene transcription + iron absorption/transport; ACE inhibitors can also cause anaemia
  • CKD-MBD detail — formerly renal osteodystrophy; ↓ PO4 excretion → ↑ plasma PO4; ↓ 25(OH)D→1,25(OH)₂D conversion → ↓ Ca absorption → hypocalcaemia; FGF23 (from osteocytes) rises to promote phosphate excretion; bone morphologies: hyperparathyroid, osteomalacia, osteoporosis, osteosclerosis, adynamic
Epidemiology/Risk
  • Risk factors — older age, heart disease/HTN, diabetes, obesity, systemic inflammatory/autoimmune disease, malignancy (e.g. multiple myeloma), family history/inherited disorders, drugs/nephrotoxins
Background
  • Cause detail — congenital (PKD, medullary cystic disease, tuberous sclerosis, oxalosis/cystinosis); vascular hypertensive nephrosclerosis (common in black African descent), renovascular disease, vasculitis; obstructive (calculi, prostatic disease, pelvic tumours, retroperitoneal fibrosis, schistosomiasis)
Other
  • Other systemic complications — delayed gastric emptying, reflux/gastritis/peptic ulcer/GI bleed, constipation (esp. CAPD), acute pancreatitis; hyperprolactinaemia, ↓ testosterone, menstrual irregularity, impaired growth in children, hypothyroidism; porphyria cutanea tarda (blistering photosensitive rash); hypercholesterolaemia

UTI & Pyelonephritis

4 entries
34

Cystitis (Uncomplicated UTI)

C/P
  • Lower UTI symptoms — dysuria, frequency, urgency
  • Suprapubic tenderness
  • Haematuria + proteinuria on urinalysis
  • Uncomplicated = premenopausal, non-pregnant woman, no tract abnormality, no significant comorbidity
  • E. coli 80%; also Klebsiella; Candida in immunocompromised/diabetic
  • Other uropathogens — Staphylococcus saprophyticus, Enterococci, Group B streptococcus, Proteus / other coliforms (Serratia, Enterobacter), Pseudomonas aeruginosa
Inves
  • Urine dipstick — +ve leucocyte esterase (WBCs) + +ve nitrite (bacterial nitrate reduction) + blood + protein
  • Microscopy — pyuria >10 WBCs/mm³; WBC casts
  • Urine culture — threshold ≥10⁵ CFU/mL; not indicated in most uncomplicated cystitis; culture if upper tract signs, atypical symptoms, high-risk patient, MDRO risk, or no improvement in 48–72 h
  • Sensitivity testing — tailor antibiotic if culture done
Mng
  • Empirical broad-spectrum antibiotic until sensitivities available
  • Lower UTI (male/non-pregnant female) — Trimethoprim PO or Nitrofurantoin PO
  • Pregnancy lower UTI — Nitrofurantoin PO or Cefalexin PO; Trimethoprim only in 2nd/3rd trimester
  • Fungal (Candida) — Fluconazole + improve immune status/glycaemic control
  • Asymptomatic bacteriuria — DO NOT treat except in pregnancy (treat as uncomplicated cystitis)
  • Catheter-related bacteriuria — treat only if symptomatic, remove catheter if possible
Special
  • Spermicides — kill protective lactobacilli of urogenital biofilms → ↑UTI risk
  • Automatically complicated — children, pregnant women, tract abnormalities, comorbidities (diabetes/CKD/immunocompromised), recent instrumentation
physiology · background · low-yield
Epidemiology/Risk
  • Women >10× more affected — short female urethra (4 cm vs 25 cm in males); risk associations include sexual intercourse, spermicides, postmenopausal state (low oestrogen ↓ protective lactobacilli), abnormal renal tract and indwelling catheter
  • Asymptomatic bacteriuria is considered normal in the >65 year age group
Microbiology
  • Significant bacteriuria = >10⁵ CFU/mL of a single organism; urine is normally sterile except at the anterior urethra
  • Full uropathogen list — E. coli (>80%), other coliforms (Klebsiella, Serratia, Enterobacter, Proteus), Enterococci, Group B Streptococcus, Staphylococcus saprophyticus, Candida albicans, Pseudomonas aeruginosa
Physiology
  • Host defences — acidic urine pH, high osmolality, mechanical flushing of flow, mucosal IgA + mucopolysaccharide lining, and in males a longer urethra with bactericidal zinc in prostatic secretions; protective vaginal lactobacilli produce H₂O₂/lactic acid and act as a biosurfactant
Mechanism
  • Uropathogenic E. coli use type 1 pili/fimbriae to bind uroplakin, invade and replicate into an intracellular bacterial community (IBC), then exfoliate/filament; bacterial toxins inhibit ureteric peristalsis to aid ascension
35

Acute Pyelonephritis

C/P
  • Upper UTI — fever, vomiting, flank pain / CVA (renal angle) tenderness
  • Dysuria; pyuria + bacteriuria on urinalysis
  • Ascending infection (commonest — E. coli, Proteus, enterobacteria) or haematogenous (rare — Staph, E. coli; septicaemia / IE / debilitated patients)
  • Systemic upset — high fever with shaking chills (rigors) and nausea
Inves
  • Urinalysis — WBC casts (proves renal origin), pyuria, positive nitrite/leucocyte esterase
  • Urine culture — organism + sensitivities
  • Bloods — ↑WBC + ↑serum creatinine; blood cultures if septic
  • Imaging — ultrasound to exclude obstruction/complications; CT if severe/complicated
Mng
  • Empirical broad-spectrum antibiotic then tailor
  • Upper UTI (male / non-pregnant female) — Fluoroquinolones PO or 3rd-gen Cephalosporin IV then PO
  • Upper UTI (pregnant) — Ceftriaxone IV or Cefotaxime IV or Ampicillin + Gentamicin IV
  • Supportive — rehydration with 0.9% NaCl, analgesia, antipyretic, antiemetics
  • Address obstruction if present (stones, catheter, prostate)
Special
  • WBC casts — form in tubules; pathognomonic evidence infection is renal (not just bladder)
  • Glomeruli resistant to bacterial damage (except large / fungal infections)
  • Complications — pyonephrosis, papillary necrosis (especially diabetics + obstruction), perinephric abscess, progression to chronic pyelonephritis
physiology · background · low-yield
Other
  • Morphology — patchy interstitial suppurative inflammation + tubular necrosis; neutrophils (PNLs) first fill the interstitium then infiltrate the tubules (PCT→DCT), which are destroyed to form microabscesses
Mechanism
  • Ascension cascade — colonisation → uroepithelial penetration → ascension → pyelonephritis → tubular obstruction + interstitial oedema → interstitial nephritis / AKI
Microbiology
  • Differential of pyuria — sterile pyuria suggests TB (Mycobacterium tuberculosis); Group A streptococcus causes post-streptococcal GN rather than direct UTI; Cryptococcus/Mycoplasma are rare urinary pathogens
  • Mycobacterium tuberculosis — causes rare sterile pyuria (haematogenous UTI organisms = S. aureus, TB)
36

Chronic Pyelonephritis

C/P
  • Shrunken deformed kidney from recurrent infections
  • Chronic obstructive form — recurrent infection on obstruction; unilateral or bilateral
  • Chronic reflux form — infection on VUR / intrarenal reflux
  • Progressive CKD; hypertension
Inves
  • Ultrasound / CT — polar scars if reflux-associated; deformity of pelvi-calyceal system; unequal contraction if bilateral
  • MCUG — confirm VUR in children
  • DMSA — split function + scarring
  • Renal biopsy — tubular "thyroidisation" (dilated tubules with colloid casts), fibrosis, diffuse lymphocytic infiltrate, periglomerular fibrosis progressing to FSGS, arteriolosclerosis from associated hypertension
Mng
  • Treat/prevent recurrent UTIs — long-term low-dose prophylactic antibiotics if severe
  • Correct underlying obstruction / VUR — surgical if severe
  • Manage as CKD — BP control (ACE-i/ARB), renoprotection
Special
  • Polar scars → reflux; non-polar → haematogenous spread
  • Tubular thyroidisation — pathognomonic microscopic pattern
  • Bilateral disease highly asymmetric (unlike glomerular disease)
physiology · background · low-yield
Mechanism
  • Reflux scarring localises because intra-renal reflux enters ducts at the tips of the renal papillae (upper & lower poles); gross scarring may be diffuse or patchy
37

Pyonephrosis / Hydronephrosis

C/P
  • Hydronephrosis — marked distension of pelvis + calyces by urine due to obstruction
  • Pyonephrosis — total obstruction + suppurative exudate that fails to drain (fills calyces + ureter)
  • Sepsis + AKI if pyonephrosis untreated
Inves
  • Ultrasound — enlarged bossy kidney; multilocular sac filled with urine (hydro) or pus (pyo)
  • CT — better delineates cause of obstruction (stone, tumour, retroperitoneal fibrosis)
  • Urine culture — if pus drained
  • Blood cultures + inflammatory markers — if septic
Mng
  • Percutaneous nephrostomy — urgent drainage for pyonephrosis (limb-of-life)
  • IV broad-spectrum antibiotics + resuscitation for sepsis
  • Definitive — relieve cause of obstruction (stone removal, stent, tumour treatment)
Special
  • Enlarged kidney with bossy outer surface + multilocular sac on cross-section

Stones & Reflux

2 entries
38

Kidney Stones (Nephrolithiasis)

C/P
  • Sudden onset, extremely severe colicky loin-to-groin pain (± testicle in male)
  • Nausea + vomiting
  • Haematuria (microscopic or overt); apyrexial (unless infected)
  • Stone types — Calcium (75%, mostly oxalate), Struvite (Ca-Mg-phosphate, chronic infection with Gram-negative urea-splitters — staghorn), Uric acid (25% have gout), Cystine
Inves
  • Urinalysis — blood on dipstick
  • Non-contrast CT KUB — gold standard; low-dose, no contrast; identifies radiopaque calculus as hyperdense focus
  • Ultrasound — echobright stone with posterior acoustic shadowing + ipsilateral hydronephrosis; bladder/VUJ stones well-seen; mid-ureteric stones poorly seen
  • Metabolic screen for recurrent stones — 24 h urine (Ca, oxalate, urate, citrate), serum Ca/PTH/urate
  • Stone analysis — determine type for prevention
Mng
  • Analgesia — NSAIDs first line; IV fluids
  • Medical expulsive therapy — for distal ureteric stones
  • <8 mm — pass spontaneously
  • Lithotripsy — only if stone is radiopaque (shockwaves)
  • Ureteroscopy — for definitive removal
  • Ureteric stenting — temporary decompression
  • Percutaneous nephrolithotomy — staghorn / large stones
  • Nephrostomy — obstructed infected system
  • Open nephrotomy — reserved for complex cases
Special
  • Struvite stones (Ca-Mg-phosphate) — chronic infection with Gram-negative urea-splitting organisms (Proteus); form staghorn calculi
  • Uric acid stones — 25% of uric acid stone patients have gout; radiolucent (not seen on X-ray)
physiology · background · low-yield
Epidemiology/Risk
  • Stone-forming risk factors — disturbances in urinary pH, low urine volume, poor fluid intake, dietary factors
Mechanism
  • Mechanism — excess of crystal-forming substances that cannot be dissolved in urine
39

Vesico-Ureteric Reflux (VUR)

C/P
  • Historically the commonest cause of renal failure
  • Young infant with UTI — E. coli commonest organism
  • Antenatal renal pelvis dilatation is a major red flag
  • Recurrent pyelonephritis → reflux nephropathy → CKD
Inves
  • Investigate all children with antenatal renal pelvis dilatation
  • Image after any proven UTI in the 1st year of life, or a UTI in boys at any age
  • Imaging sequence: US → MCUG → DMSA
  • Ultrasound — dilated renal pelvis / ureter
  • MCUG (Micturating Cystourethrogram) — demonstrates retrograde flow of contrast from bladder into ureters/kidneys
  • DMSA scan — assess for renal cortical scarring + split function
  • Grade 1–5 (see Criteria tab)
Mng
  • Low-dose prophylactic antibiotics — 3–5 years
  • Follow-up US ± DMSA — monitor growth + split function
  • Consider surgery if severe (higher grades, breakthrough infection despite prophylaxis)
  • Most children grow out of it
Special
  • Early detection + prophylaxis prevents recurrent pyelonephritis → renal scarring / reflux nephropathy

Renal Neoplasms

2 entries
40

Renal Cell Carcinoma (RCC)

C/P
  • Older adult with painless haematuria + PUO (paraneoplastic fever)
  • Solid necrotic renal mass on imaging
  • Most common solid renal lump (~90%)
Inves
  • Ultrasound — well-defined globular mass lesion at renal pole
  • Post-contrast CT abdomen/pelvis — soft tissue mass with central hypodense area (necrosis from outgrowing blood supply); staging (spread to adjacent tissues, liver/lungs/bones, renal vein/IVC involvement, baseline for follow-up)
  • Urinalysis — haematuria
  • MR — for angiomyolipoma / associated abnormalities
Mng
  • Surgical resection (radical or partial nephrectomy)
  • Embolisation of the vascular tumour — palliation or preoperative adjunct
Special
  • Renal vein / IVC tumour thrombus — characteristic behaviour on CT
  • Associated cystic syndromes — polycystic kidney disease, von Hippel-Lindau
physiology · background · low-yield
Background
  • Differential of solid renal lumps also includes transitional cell Ca, squamous cell Ca, leukaemia/lymphoma, metastases, and benign tumours (angiomyolipoma, Wilms, oncocytoma)
41

Urothelial Carcinoma (TCC)

C/P
  • Haematuria (painless)
  • Can occur anywhere along urothelium — renal pelvis, ureter, bladder
Inves
  • Urography — filling defect + stenotic appearance; multiple filling defects strongly suggest carcinoma rather than stones
  • Bladder TCC — well-defined mass lesion within the bladder on ultrasound and on axial CT pelvis
Mng
  • Surgical resection appropriate to site (per urology)
Special
  • Multiple filling defects → probably carcinoma rather than stones

Renal Replacement Therapy

1 entry
42

Renal Replacement Therapy (HD / PD / Transplant)

C/P
  • Indicated in ESRD (irreversible) or severe AKI meeting AEIOU criteria
  • Three modalities — haemodialysis, peritoneal dialysis, renal transplantation
  • Urgent AKI dialysis indications (AEIOU) — refractory fluid overload, refractory metabolic acidosis, hyperkalaemia, alcohol/drug intoxications, uraemia (pericarditis, neuropathy, encephalopathy)
  • CKD dialysis indications — uraemic symptoms (nausea, anorexia, cognitive impairment; nutritional deterioration refractory to diet) + electrolyte derangement (hyperkalaemia, hyperphosphataemia, hypocalcaemia)
Inves
  • Confirm need — GFR + symptoms; screen contraindications
  • Transplant workup — HLA typing, crossmatch, virology (HBV/HCV/HIV/CMV/EBV), cardiovascular fitness, imaging
  • Dialysis workup — vascular mapping (Doppler US) for AV fistula; abdominal assessment for PD suitability
Mng
  • Haemodialysis (HD) — semipermeable dialyser + dialysate; solutes cleared via diffusion + ultrafiltration; vascular access = AV fistula (preferred), AV graft, venous catheter (temporary/highest complication risk); complications thrombosis + infection
  • HD types — IHD 3–5 h sessions for haemodynamically stable; CRRT ~24 h for haemodynamically unstable ICU patients (gentle gradual clearance)
  • Peritoneal dialysis (PD) — dialysate flows via catheter into peritoneum → peritoneum acts as filter; diffusion + ultrafiltration; fluid drained after dwell
  • PD absolute contraindications — peritoneal adhesions from previous surgery (heavily tested), surgically uncorrectable abdominal hernia, abdominal wall stoma (colostomy), diaphragmatic fluid leak, inability to perform exchanges
  • HD absolute contraindication — no vascular access possible (recurrent thrombosis, severe atherosclerosis)
  • Renal transplantation — treatment of choice for ESRD; more physiological + better QoL + better long-term survival than dialysis; placed in iliac fossa; deceased-donor or living-donor
  • Pre-emptive transplant — GFR < 20 without symptoms; asymptomatic + no contraindications → straight to transplant
  • Transplant contraindications (all 6) — active sepsis, current uncontrolled malignancy, uncontrolled psychosis, active drug dependence, severely shortened life expectancy (<1–2 y), recipient immunologically incompatible with donor
  • Post-transplant immunosuppression — mandatory; balance rejection vs infection/malignancy side effects
  • Decision algorithm — CKD asymptomatic: contraindications → HD/PD else pre-emptive transplant; CKD symptomatic: start IHD then transplant if eligible; AKI: no urgent indication → medical; urgent → IHD if stable, CRRT if unstable
  • Vascular access — AV fistula needs 1–4 weeks to mature before it can be used; venous catheter bridges the acute need in the interim
Special
  • PD may be preferred in children
  • Long-term HD — β₂-microglobulin amyloidosis → carpal tunnel syndrome
  • Uraemia as a dialysis indication is symptom-dependent, not number-dependent — the urea level itself doesn't mandate dialysis without symptoms
physiology · background · low-yield
Mechanism
  • HD circuit has 4 components — vascular access, dialyser (filter), dialysate, HD machine; only water + LMW solutes cross the membrane pores
Background
  • HD-vs-PD choice depends on 3 factors — patient preference/will, availability of the procedure, absence of contraindications
Other
  • Isolated lecturer handwritten note in the decision algorithm — HBV is stated to be “the only thing that gets transmitted” (context not further specified on the slide)
Other
  • Full AKI RRT modality list also includes haemodiafiltration (HDF) and continuous venovenous haemofiltration (CVVHF) alongside IHD, CRRT and PD

Additions — Approach & OSCE

4 entries
43

Nephrotic Syndrome (Complications & General Management)

C/P
  • Definition — proteinuria >3.5 g/day + serum albumin <3.5 g/dL + generalised oedema (± hyperlipidaemia, lipiduria)
  • Hyperlipidaemia + lipiduria — hypoalbuminaemia drives reactive hepatic lipoprotein synthesis; filtered lipoproteins appear as oval fat bodies and fatty casts in the sediment
  • Hypercoagulability — urinary loss of natural anticoagulants (antithrombin III, plasminogen, protein C & S) → DVT, renal vein thrombosis, PE
  • Infection (sepsis, peritonitis, cellulitis) — urinary loss of IgG + alternative-pathway complement, fluid collections, fragile skin
  • Negative nitrogen balance — heavy proteinuria → muscle wasting
  • AKI — pre-renal / ATN (volume depletion), renal vein thrombosis, or drug adverse effects
Mng
  • ACE-i / ARB — efferent arteriolar vasodilation → ↓ intraglomerular pressure → ↓ proteinuria; first choice for hypertension
  • Oedema / HTN — dietary sodium restriction + loop diuretic ± thiazide; target BP <130/80
  • Adequate dietary protein 0.8–1 g/kg/day to replace urinary loss
  • Hyperlipidaemia — statin (HMG-CoA reductase inhibitor) ± ezetimibe (blocks intestinal cholesterol absorption)
  • Hypercoagulability — prophylactic anticoagulation (heparin, warfarin)
  • Infection — parenteral antibiotics
44

Diuretics — Sites & Mechanisms of Action

Special
  • Thiazides — block the Na-Cl cotransporter in the distal convoluted tubule (DCT); inhibit Na/Cl/water reabsorption
  • Loop diuretics — block the Na-K-2Cl cotransporter in the thick ascending limb of the loop of Henle; inhibit Na/Cl/K/water reabsorption; ↑ urinary K loss; water loss > Na loss
  • Potassium-sparing (aldosterone antagonists) — act on the distal tubules, antagonise aldosterone; produce diuresis without increasing urinary K loss
45

Renal Imaging Modalities (Approach)

Inves
  • Ultrasound — first-line; assesses number, size, shape (smooth vs scarred), calcification; sees bladder + kidney but not the ureters (obscured by bowel gas)
  • Plain film (KUB / PUT) — radiopaque stones; needs bowel prep (enema, avoid gassy foods)
  • IVU / IVP — X-ray with contrast; shows backpressure changes; radiolucent stones appear as filling defects
  • CT UT — "golden modality," high radiation but no contrast, detects stones and virtually everything; CT urography = CT UT + contrast
  • Isotope scan (renogram) — DTPA (fewer hazards) / MAG3 tracers; measures GFR + split function; captopril challenge exposes renovascular disease
  • MRI — tissue characterisation, tumour localisation, angiomyolipoma; poor for stones
physiology · background · low-yield
Other
  • Renal cyst characterisation — simple (thin-walled, no enhancement = benign) vs complex (nodules, thick wall, septations = suspicious); ~5% of cysts malignant; associated with PKD and von Hippel-Lindau; benign normal "lumps" = fetal lobulation, dromedary hump
  • Interventional (fluoroscopy) — dilatation/stenting of stenoses, embolisation of vascular tumours or bleeding vessels, nephrostomy / stent insertion
46

UTI Pathogenesis & Host Defences

physiology · background · low-yield
Microbiology
  • Host defences — urine (acidic pH, high osmolality, mechanical flushing, adherence inhibitors); mucosa (secretory IgA, cytokines/chemokines, mucopolysaccharide lining); males (longer urethra, bactericidal zinc in prostatic secretions)
  • Protective biofilm — urogenital cells coated by dense biofilms in which lactobacilli predominate; they produce H₂O₂ + lactic acid, act as a biosurfactant and block pathogen adhesion; disrupted by low oestrogen, oral contraception, steroids/immunosuppression, diabetes
  • E. coli virulence — gram-negative enterobacteria; type 1 pili / fimbriae bind uroplakin → invade → form an intracellular bacterial community (IBC) → exfoliation + filamentation
  • Progression — colonisation → uroepithelial penetration → ascension (bacterial toxins inhibit peristalsis) → pyelonephritis → interstitial nephritis / AKI; routes = ascending (perineal flora, commonest) vs haematogenous (S. aureus, TB — rare)

Diagnostic Criteria

2 entries
1

KDIGO — CKD Diagnostic Criteria

Definition: Longstanding (>3 months), potentially progressive impairment in renal function.

Criteria (either present for >3 months)
  • GFR < 60 mL/min/1.73 m² (GFR categories G3a–G5), OR
  • One or more markers of kidney damage:
    • Albuminuria — AER >30 mg/24 h; ACR >30 mg/g or >3 mg/mmol
    • Urine sediment abnormalities
    • Electrolyte / tubular abnormalities (tubular disorders)
    • Histological abnormalities
    • Structural abnormalities on imaging
    • History of kidney transplantation
2

ADPKD — Ultrasound Diagnostic Criteria

Context: Patients with positive family history of ADPKD.

AgeDiagnostic threshold
< 30 yTwo cysts (unilateral or bilateral)
30–59 yTwo cysts in both kidneys
≥ 60 yFour cysts in both kidneys

Criteria become stricter with age because simple renal cysts are common in older healthy individuals.

AKI Staging Systems

3 entries
3

RIFLE Criteria

5 stages: Risk · Injury · Failure · Loss · End-stage renal disease.

StageSerum creatinineUrine output
RisksCr × 1.5 or ≥0.3 mg/dL<0.5 mL/kg/h × 6 h
InjurysCr × 2<0.5 mL/kg/h × 12 h
FailuresCr × 3 or ≥0.5 mg/dL if baseline >4.0 mg/dL<0.3 mL/kg/h × 24 h or anuria × 12 h
LossComplete loss of renal function > 4 weeks
ESRDEnd-stage renal disease
4

AKIN Criteria

Mirrors first 3 grades of RIFLE, strips out outcome classes (Loss/ESRD).

StageSerum creatinineUrine output
Stage 1sCr × 1.5 or ≥0.3 mg/dL<0.5 mL/kg/h × 6 h
Stage 2sCr × 2<0.5 mL/kg/h × 12 h
Stage 3sCr × 3 or ≥0.5 mg/dL if baseline >4.0 mg/dL<0.3 mL/kg/h × 24 h or anuria × 12 h

Patients who receive RRT are considered to have met stage 3 criteria, irrespective of the stage they were in at the time of RRT.

5

KDIGO AKI Staging

Merges RIFLE + AKIN with baseline SCr multipliers and paediatric criteria.

StageSerum creatinineUrine output
Stage 1SCr 1.5–1.9 × baseline OR ≥26.5 µmol/L (0.3 mg/dL) increase<0.5 mL/kg/h for 6–12 h
Stage 2SCr 2–2.9 × baseline<0.5 mL/kg/h for 6–12 h
Stage 3SCr 3 × baseline OR initiation of RRTAnuria for ≥12 h

< 18 y: Decrease in eGFR to <35 mL/min/1.73 m²

CKD Staging

2 entries
6

KDIGO — GFR & ACR Categories

GFR Categories (mL/min/1.73 m²)
StageGFRDescription
G1≥ 90Normal or ↑ GFR with other evidence of kidney damage
G260–89Slight decrease in GFR with other evidence of kidney damage
G3a45–59Moderate decrease in GFR (± other evidence)
G3b30–44Moderate to severe decrease in GFR
G415–29Severe decrease in GFR (± other evidence)
G5< 15End-stage renal disease → dialysis
ACR Categories (mg/mmol)
CategoryACR
A1< 3
A23–30
A3> 30

Risk of adverse outcomes increases as GFR ↓ and ACR ↑ (matrix combines both dimensions).

7

eGFR Equations (CKD-EPI & MDRD)

Estimated GFR (eGFR)
  • CKD-EPI — most widely used, more accurate at high GFR
  • MDRD — older, less accurate at high GFR
  • Markers used — serum creatinine + cystatin C
  • Clinical use — routine kidney function assessment, KDIGO CKD staging, drug dosing
  • Limitations — influenced by age, sex, muscle mass, diet, drugs; less accurate at extremes of body size, muscle wasting, pregnancy
Measured GFR (mGFR)
  • Gold standard — inulin clearance
  • Others — radioisotopes (⁵¹Cr-EDTA, iohexol); 24 h creatinine clearance
  • Endogenous — creatinine (24 h clearance)
  • Exogenous — inulin, iohexol, radioisotopes
  • Use — research, transplant donor assessment, individual kidney function
  • Limitations — time-consuming, expensive, not practical for routine
Other Blood Markers
  • Serum creatinine — most common estimate; affected by muscle mass, diet, drugs
  • BUN — less specific; ↑ with dehydration, high protein diet
  • Cystatin C — less influenced by muscle mass than creatinine

Histological Classifications

2 entries
8

Lupus Nephritis — 6 Classes

ClassNameDistinguishing feature
IMinimal mesangialMinimal changes only
IIMesangial proliferativeMesangial hypercellularity
IIIFocalFocal (<50% glomeruli); sub-endothelial deposits
IVDiffuseDiffuse (≥50% glomeruli); crescent formation; sub-endothelial deposits
VMembranousSub-epithelial deposits; thickened GBM on silver stain
VIAdvanced sclerosisGlobal glomerulosclerosis
Deposit locations by class
  • Sub-endothelial — Classes III + IV (focal and diffuse proliferative)
  • Mesangial — Classes I–V
  • Sub-epithelial — Class V (membranous)
9

RPGN — 3 Types by IF Pattern

TypeIF PatternDiseases
Type ILinear depositsIdiopathic; Goodpasture's (anti-GBM)
Type IIGranular (immune complex)Idiopathic; SLE; post-infective
Type IIIPauci-immuneIdiopathic; Wegener's granulomatosis; Polyarteritis nodosa (PAN)

All three classified together clinically because they present with rapid loss of renal function + crescent formation on biopsy, regardless of underlying cause.

Anatomical / Severity

1 entry
10

VUR — 5 Grades

GradeFeatures
Grade 1Reflux limited to the ureter
Grade 2Reflux up to the renal pelvis (no dilatation)
Grade 3Mild dilatation of ureter + pelvicalyceal system
Grade 4Tortuous ureter with moderate dilatation, blunting of fornices but preserved papillary impressions
Grade 5Tortuous ureter with severe dilatation of ureter + pelvicalyceal system with loss of fornices and papillary impressions

Low grades often resolve spontaneously; Grades 4 + 5 more likely to require surgical correction.

Urine Chemistry & Sediment

2 entries
11

Pre-renal vs Intrinsic AKI — Urine Chemistry

ParameterPre-renalIntrinsic
Urine specific gravity> 1.020< 1.010
Urine osmolality (mosm/kg)> 500< 350
Urine sodium (mmol/L)< 10> 20
FENa< 1%> 1%
BUN : Creatinine> 20 : 1< 20 : 1
Urea : Creatinine> 40 : 1< 40 : 1
FENa Formula

FENa = [(urinary Na × serum creatinine) / (urinary creatinine × serum Na)] × 100

In pre-renal states the kidney conserves salt + water (low Na, high osm). ADH-mediated water/urea reabsorption drives the disproportionate BUN rise.

12

Urinary Casts — 7 Types

Casts form in kidney tubules; the content of a cast reflects the type of renal lesion (proves the process is renal, not lower-tract).

TypeAssociation
Fatty castsNephrotic syndrome
Granular castsNonspecific — many kidney disorders, especially ATN
Hyaline castsDehydration, exercise, diuretics (few normal)
RBC castsGlomerular bleeding — IgA nephropathy, lupus nephritis, Goodpasture's, vasculitis
Renal tubular epithelial cell castsRenal tubular necrosis, viral disease, kidney transplant rejection
WBC castsInterstitial kidney disease — interstitial inflammation, pyelonephritis, parenchymal infection
Waxy castsAdvanced kidney disease + chronic kidney failure