{"title": "Chapter 7: Kidney Disease and Electrolyte Disorders", "flashcards": [{"q": "Define AKI using KDIGO 2012 staging criteria.", "a": "AKI Stage 1: creatinine rise 1.5–1.9× baseline within 7 days, OR ≥26.5 µmol/L rise in 48h, OR UO <0.5 mL/kg/h for 6–12h. Stage 2: creatinine 2–2.9× baseline or UO <0.5 mL/kg/h for ≥12h. Stage 3: ≥3× baseline, OR creatinine ≥353.6 µmol/L, OR initiation of RRT, OR UO <0.3 mL/kg/h for ≥24h."}, {"q": "What is the AEIOU mnemonic for emergency dialysis indications?", "a": "Acidosis (metabolic pH <7.1 refractory to treatment); Electrolytes (hyperkalaemia refractory to medical management); Intoxication (lithium, methanol, salicylates); Overload (pulmonary oedema refractory to diuretics); Uraemia (encephalopathy, pericarditis, bleeding diathesis). Presence of any indication warrants urgent nephrology input."}, {"q": "What urine electrolyte pattern distinguishes prerenal from intrinsic AKI?", "a": "Prerenal: FENa <1%, urine Na <20 mmol/L, urine osmolality >500 mOsm/kg (intact tubular avid Na⁺ reabsorption). ATN (intrinsic): FENa >2%, urine Na >40 mmol/L, urine osmolality ~300 mOsm/kg (tubular injury impairs reabsorption). FENa is unreliable if diuretics given; use FEUrea <35% as alternative in diuretic-treated patients."}, {"q": "Name four causes of hypokalaemia with metabolic alkalosis.", "a": "Vomiting/NG suction (loss of HCl → metabolic alkalosis + urinary K⁺ wasting); primary hyperaldosteronism (Conn's syndrome — hypertension, hypokalaemia, metabolic alkalosis); diuretics (loop and thiazides — urinary K⁺ wasting); Bartter's syndrome; Gitelman's syndrome; Cushing's syndrome."}, {"q": "What is the most important step in managing severe symptomatic hyponatraemia?", "a": "For seizures or coma from acute hyponatraemia: IV hypertonic saline (3% NaCl), targeting 1–2 mmol/L/hour rise, with absolute maximum correction of 10–12 mmol/L in first 24 hours and 18 mmol/L in 48 hours. Overcorrection risks osmotic demyelination syndrome (central pontine myelinolysis). Correct the underlying cause simultaneously."}, {"q": "Define nephrotic syndrome and its four cardinal features.", "a": "Proteinuria >3.5 g/24h (or PCR >350 mg/mmol), hypoalbuminaemia (<25 g/L), oedema, and hyperlipidaemia/lipiduria. Causes: minimal change disease (children), membranous nephropathy (adults), FSGS, diabetic nephropathy, amyloidosis. Complications: thromboembolism (renal vein thrombosis, PE — especially membranous), infection (lost immunoglobulins), AKI, malnutrition."}, {"q": "What is the mechanism of renal tubular acidosis type 1 (distal)?", "a": "Distal RTA (type 1): failure of H⁺ secretion in the alpha-intercalated cells of the distal tubule. Unable to acidify urine below pH 5.5 even with severe acidaemia. Results in: normal AG metabolic acidosis, hypokalaemia (K⁺/H⁺ exchange), nephrocalcinosis, nephrolithiasis (calcium phosphate stones). Causes: Sjögren's syndrome, amphotericin toxicity, SLE."}, {"q": "What is the management of hypermagnesaemia with neuromuscular toxicity?", "a": "IV calcium gluconate 10% (10 mL slowly IV) antagonises magnesium at the neuromuscular junction and acts within minutes. Supportive care for respiratory failure (mechanical ventilation if needed). IV furosemide + normal saline promotes renal magnesium excretion. Haemodialysis for severe toxicity or renal failure. Stop all magnesium-containing medications."}, {"q": "Name three autoimmune causes of membranoproliferative glomerulonephritis (MPGN).", "a": "SLE nephritis (Class III/IV); cryoglobulinaemia (associated with HCV infection, Waldenström's macroglobulinaemia); anti-GBM disease (Goodpasture syndrome); ANCA-associated vasculitis (GPA, MPA). MPGN shows low C3 ± C4 on complement testing; C3 nephropathy from complement dysregulation; immune complex MPGN from autoimmune disease."}, {"q": "What is the target blood pressure in CKD with proteinuria?", "a": "<130/80 mmHg per KDIGO 2021 CKD guidelines for patients with proteinuria (ACR >30 mg/mmol). ACE inhibitors or ARBs are first-line in CKD with proteinuria to reduce intraglomerular pressure and slow progression. SGLT2 inhibitors (dapagliflozin, empagliflozin) now have strong evidence for renoprotection in CKD (DAPA-CKD, EMPA-KIDNEY trials)."}], "quiz": [{"q": "What is the immediate management of hyperkalaemia with ECG changes (peaked T waves, wide QRS)?", "opts": ["Dietary potassium restriction alone", "IV calcium gluconate 10% (membrane stabilisation) → insulin-dextrose → sodium bicarbonate if acidotic → dialysis", "Oral potassium binders alone", "IV sodium bicarbonate as sole treatment"], "ans": 1, "exp": "Sequence for emergency hyperkalaemia: (1) IV calcium gluconate 10 mL 10% over 5–10 min — membrane stabilisation, acts within minutes, repeat if no ECG improvement; (2) Insulin 10U actrapid + 50 mL 50% glucose — shifts K⁺ intracellularly (onset 15–30 min); (3) Sodium bicarbonate if severe acidosis; (4) Definitive K⁺ removal: dialysis (fastest), sodium zirconium cyclosilicate (SZC), patiromer, or Resonium A."}, {"q": "Which investigation best monitors lupus nephritis activity?", "opts": ["Serum creatinine only", "Anti-dsDNA antibody titres, complement C3/C4, and quantitative proteinuria (PCR or ACR)", "Anti-GBM antibody", "Serum ANA titre"], "ans": 1, "exp": "Lupus nephritis activity is monitored with: anti-dsDNA (rises with flares), complement (C3/C4 fall in active nephritis from immune complex consumption), PCR/ACR (proteinuria quantification), urine microscopy (cellular casts), and eGFR. Renal biopsy is required for histological classification (ISN/RPS Classes I–VI) to guide immunosuppressive therapy."}, {"q": "A 45-year-old with type 2 diabetes and eGFR 35 is started on dapagliflozin. What is the primary renoprotective mechanism?", "opts": ["Reduces blood glucose exclusively", "Reduces intraglomerular pressure via SGLT2 inhibition reducing tubuloglomerular feedback and afferent arteriolar dilation; also reduces albuminuria and blood pressure independent of glycaemic effect", "Reduces blood pressure only", "Reduces weight only"], "ans": 1, "exp": "SGLT2 inhibitors reduce glucose and sodium reabsorption in the proximal tubule. The resulting increased macula densa sodium delivery restores tubuloglomerular feedback, causing afferent arteriolar constriction → reduced intraglomerular pressure → reduced hyperfiltration. This mechanism, independent of glycaemic control, reduces albuminuria and GFR decline. DAPA-CKD showed 39% relative risk reduction in CKD progression."}, {"q": "What is the diagnostic hallmark of anti-GBM disease (Goodpasture syndrome) on renal biopsy?", "opts": ["Mesangial IgA deposits", "Linear IgG deposits along the glomerular basement membrane on immunofluorescence", "Subepithelial 'spike and dome' deposits", "Segmental glomerulosclerosis"], "ans": 1, "exp": "Anti-GBM disease shows linear IgG (and C3) staining along the GBM on immunofluorescence — the pathognomonic finding distinguishing it from MPGN or FSGS. Serum anti-GBM antibody confirms the diagnosis. Pulmonary haemorrhage + rapidly progressive GN = Goodpasture syndrome. Treatment: plasma exchange (14 sessions) + prednisolone + cyclophosphamide."}, {"q": "What is the urinalysis finding most specific for glomerulonephritis?", "opts": ["2+ proteinuria on dipstick", "Red cell casts on phase-contrast microscopy", "White cells in urine", "Glucose in urine without hyperglycaemia"], "ans": 1, "exp": "Red cell (erythrocyte) casts form when RBCs enter the tubular lumen through glomerular damage and are encased in Tamm-Horsfall mucoprotein. They are pathognomonic of glomerulonephritis (haematuria of glomerular origin). Dysmorphic red cells (acanthocytes) additionally confirm glomerular haematuria."}, {"q": "What is the key difference between haemodialysis and peritoneal dialysis?", "opts": ["PD is more efficient than HD", "HD uses an extracorporeal blood circuit through a semipermeable membrane; PD uses the peritoneum as a dialysis membrane with dwell of dialysate within the peritoneal cavity, allowing home-based treatment", "PD requires arteriovenous fistula", "HD cannot remove phosphate"], "ans": 1, "exp": "HD: extracorporeal circulation through a dialyser (semipermeable membrane), typically 3× weekly in a dialysis unit; highly efficient. PD: dialysate instilled into the peritoneal cavity via a Tenckhoff catheter; the peritoneum acts as a semipermeable membrane; continuous ambulatory PD (CAPD) or automated PD (APD) allows home treatment; better preserves residual renal function."}, {"q": "A 55-year-old man has Na⁺ 118 mmol/L and is asymptomatic. What is the appropriate correction rate?", "opts": ["Correct to normal in 6 hours with IV 3% NaCl", "Correct by no more than 8–10 mmol/L per 24 hours with 0.9% saline, address underlying cause", "Restrict fluids only", "No treatment needed as asymptomatic"], "ans": 1, "exp": "Chronic asymptomatic hyponatraemia (onset >48 hours or unknown) must be corrected slowly to prevent osmotic demyelination syndrome: maximum 8–10 mmol/L in 24 hours, and 18 mmol/L in 48 hours. Treatment: fluid restriction (SIADH), salt tablets or 0.9% saline (hypovolaemia), fludrocortisone (cerebral salt wasting), tolvaptan (SIADH — specialist use). IV 3% NaCl reserved for acute symptomatic hyponatraemia."}, {"q": "Which drug is used for hyperphosphataemia in CKD and what is its mechanism?", "opts": ["Furosemide", "Calcium carbonate or sevelamer (phosphate binders taken with meals to bind dietary phosphate in the GI tract)", "Bisphosphonates", "Calcitriol"], "ans": 1, "exp": "Phosphate binders (calcium carbonate, calcium acetate, sevelamer hydrochloride, lanthanum carbonate) bind dietary phosphate in the GI tract, reducing absorption. They must be taken with meals to be effective. Sevelamer and lanthanum are calcium-free and preferred when calcium load is a concern. Phosphate restriction <800 mg/day dietary advice is complementary."}, {"q": "What are the three main types of renal calculi and which is most common?", "opts": ["Struvite, xanthine, silica", "Calcium oxalate (most common ~80%), uric acid, struvite (infection stones), cystine", "Calcium phosphate, uric acid, cystine", "Oxalate, phosphate, citrate"], "ans": 1, "exp": "Calcium oxalate stones (radiopaque) are most common (~80%). Uric acid stones (radiolucent, seen in gout/hyperuricosuria) account for ~5–10%. Struvite (magnesium ammonium phosphate — infection stones from urease-producing organisms) ~10%. Cystine stones (<1%) in cystinuria. Hydration is the cornerstone of prevention for all stone types."}, {"q": "What is membranous nephropathy and which antibody is diagnostic in primary disease?", "opts": ["Focal segmental scarring, no specific antibody", "Subepithelial immune complex deposition causing nephrotic syndrome; anti-PLA2R antibody positive in ~75% of primary cases", "Mesangial IgA, diagnosed by biopsy showing IgA deposits", "Linear GBM staining with anti-GBM antibody"], "ans": 1, "exp": "Primary membranous nephropathy is caused by in-situ immune complex formation — autoantibodies against PLA2R (phospholipase A2 receptor) on podocytes form subepithelial deposits. Anti-PLA2R titres correlate with disease activity and can monitor treatment response. Secondary causes: SLE, HBV, malignancy, drugs (NSAIDs, penicillamine). Treatment: immunosuppression for persistent heavy proteinuria or declining GFR."}, {"q": "What is the renal threshold for glucose excretion?", "opts": ["5.6 mmol/L", "Approximately 10 mmol/L plasma glucose — above which tubular maximum (Tm) for glucose reabsorption is exceeded and glycosuria occurs", "7.0 mmol/L", "14 mmol/L"], "ans": 1, "exp": "The proximal tubule reabsorbs glucose via SGLT2 (high-capacity, low-affinity) and SGLT1 (low-capacity, high-affinity). The renal threshold is approximately 10 mmol/L (180 mg/dL) — above which tubular maximum is exceeded and glucose spills into urine. SGLT2 inhibitors lower the renal threshold to ~5–6 mmol/L, inducing glucosuria at normal plasma glucose concentrations."}, {"q": "Which electrolyte disturbance causes shortened QT interval on ECG?", "opts": ["Hypokalaemia", "Hypercalcaemia", "Hypomagnesaemia", "Hyponatraemia"], "ans": 1, "exp": "Hypercalcaemia shortens the QT interval (reduced phase 2 of action potential — shortened ST segment). Hypokalaemia and hypomagnesaemia prolong the QT interval. Hyperkalaemia causes peaked T waves, widened QRS, and eventually sine wave pattern. Rapid assessment of QT interval and electrolytes is essential in arrhythmia management."}, {"q": "What is the mechanism of action of acetazolamide?", "opts": ["Loop diuretic — inhibits NKCC2", "Carbonic anhydrase inhibitor — reduces bicarbonate reabsorption in the proximal tubule, causing bicarbonate diuresis and metabolic acidosis", "Potassium-sparing — inhibits aldosterone", "Osmotic diuretic"], "ans": 1, "exp": "Acetazolamide inhibits carbonic anhydrase in the proximal tubule, reducing H⁺ secretion and HCO₃⁻ reabsorption. Results in bicarbonate diuresis, lowering serum bicarbonate and causing mild metabolic acidosis. Used for: altitude sickness prevention; metabolic alkalosis complicating COPD; glaucoma; idiopathic intracranial hypertension; periodic paralysis."}, {"q": "What is the definition of chronic kidney disease (CKD)?", "opts": ["eGFR <60 for >1 week", "eGFR <60 mL/min/1.73 m² AND/OR evidence of kidney damage (proteinuria, haematuria, structural abnormality) persisting for >3 months", "Creatinine >150 µmol/L", "Any abnormal urinalysis"], "ans": 1, "exp": "KDIGO 2012 defines CKD as: kidney damage (albuminuria ≥30 mg/g, or haematuria, or structural/histological abnormality) OR GFR <60 mL/min/1.73 m², either or both, for ≥3 months. CKD is classified by G (GFR category G1–G5) and A (albuminuria category A1–A3). The '3-month' criterion distinguishes CKD from AKI."}, {"q": "What is the most common cause of CKD in sub-Saharan Africa and South/Southeast Asia?", "opts": ["Autoimmune nephritis", "Diabetic nephropathy, hypertensive nephrosclerosis, and glomerulonephritis (especially IgA nephropathy and post-infectious GN) — with HIV-associated nephropathy (HIVAN) prominent in high-prevalence HIV regions", "Polycystic kidney disease", "Analgesic nephropathy"], "ans": 1, "exp": "Globally, the leading causes of CKD vary by region. In high-income countries: diabetic nephropathy and hypertensive nephrosclerosis dominate. In sub-Saharan Africa: HIVAN, hypertensive nephrosclerosis, and infectious GN (post-streptococcal, malaria-related). In Asia: IgA nephropathy and diabetic nephropathy. Globally, diabetes and hypertension account for >50% of ESRD cases."}, {"q": "What urine finding suggests rhabdomyolysis as a cause of AKI?", "opts": ["Casts containing RBCs", "Urine dipstick positive for blood but urine microscopy shows no red blood cells — free myoglobin cross-reacts with dipstick haemoglobin", "White cell casts", "Glucose in urine"], "ans": 1, "exp": "Rhabdomyolysis (massive muscle breakdown) releases myoglobin, which is filtered by glomeruli. Urine dipstick falsely tests positive for 'blood' (haem group cross-reactivity with myoglobin), but microscopy shows no RBCs. Serum CK is markedly elevated (often >10,000 IU/L). Causes: trauma/crush injury, prolonged seizures, statins/fibrates, alcohol, extreme exercise, hyperthermia."}, {"q": "What is the recommended dietary phosphate intake in patients with CKD stage 4–5?", "opts": ["Unrestricted phosphate intake", "Dietary phosphate restriction to approximately 800–1000 mg/day, with phosphate binders prescribed if phosphate remains elevated despite restriction", "<200 mg/day", "Only restriction when on dialysis"], "ans": 1, "exp": "CKD impairs renal phosphate excretion, leading to hyperphosphataemia (drives secondary hyperparathyroidism, renal osteodystrophy, and vascular calcification). KDIGO recommends lowering elevated phosphate toward normal range with dietary restriction (~800–1000 mg/day) and phosphate binders if dietary restriction is insufficient. Target serum phosphate 0.87–1.49 mmol/L."}, {"q": "Which imaging modality is best for detecting renal artery stenosis?", "opts": ["Renal ultrasound alone", "CT angiography or MR angiography — both visualise the renal arteries; Doppler ultrasound is a useful non-invasive screening tool; catheter angiography is the gold standard", "AXR", "Nuclear medicine DMSA scan"], "ans": 1, "exp": "Renal artery stenosis (RAS): Doppler renal ultrasound is first-line screening (resistive index, peak systolic velocity, renal-to-aortic ratio). MR angiography (avoids radiation and contrast nephropathy) or CT angiography (faster, higher resolution) for definitive diagnosis. Catheter angiography (gold standard) is reserved for when intervention (stenting or bypass) is planned."}, {"q": "What is the pathophysiology of hypocalcaemia in CKD?", "opts": ["Excess calcium in urine", "Impaired renal 1-alpha-hydroxylation of 25-OH-vitamin D → reduced 1,25(OH)₂D (active calcitriol) → decreased intestinal calcium absorption + secondary hyperparathyroidism from phosphate retention", "Hypermagnesaemia displacing calcium", "Reduced dietary calcium intake"], "ans": 1, "exp": "CKD reduces 1-alpha-hydroxylase activity in the kidney, impairing conversion of calcidiol to active calcitriol (1,25-dihydroxyvitamin D). Reduced calcitriol → decreased intestinal calcium absorption → hypocalcaemia → secondary hyperparathyroidism (PTH rises to restore calcium, causing bone resorption and phosphate release — worsening hyperphosphataemia). Treatment: calcitriol or alfacalcidol supplementation."}, {"q": "What is 'contrast-induced nephropathy' (CIN) and how is it prevented?", "opts": ["CIN is unavoidable in CKD", "AKI occurring within 48–72 hours of intravascular iodinated contrast, typically defined as creatinine rise ≥26.5 µmol/L or ≥25% from baseline; prevented by IV hydration with 0.9% NaCl before and after contrast, using low-osmolar contrast, minimising contrast volume, avoiding NSAIDs/metformin pre-procedure", "CIN occurs only with gadolinium-based contrast", "CIN risk is the same regardless of baseline eGFR"], "ans": 1, "exp": "CIN risk is highest when eGFR <45, particularly <30. Prevention: IV isotonic saline at 1 mL/kg/h for 3–12 hours pre- and 6–12 hours post-procedure. Use lowest effective contrast volume; low-osmolar or iso-osmolar iodinated contrast. Withhold NSAIDs, metformin, and renally-cleared nephrotoxins. N-acetylcysteine evidence is inconsistent and no longer routinely recommended."}]}