IM10.1-24 | Acute Kidney Injury and Chronic Renal Failure — Practice Quiz

Correct. Low urine sodium (less than 20 mEq/L) with concentrated urine indicates intact tubular reabsorption responding to volume depletion — the hallmark of pre-renal AKI. The FENa would be less than 1%. The clinical history of fluid losses from vomiting and diarrhoea confirms volume depletion as the pre-renal insult.

Pre-renal AKI: urine Na less than 20 mEq/L, FENa less than 1%, concentrated urine (SG greater than 1.020, osmolality greater than 500 mOsm/kg). Intrinsic (ATN): urine Na greater than 40 mEq/L, FENa greater than 2%, dilute urine. FENa is invalid after diuretics.

Low urine sodium (less than 20 mEq/L) and concentrated urine (high specific gravity) indicate the tubules are intact and avidly retaining sodium and water — this is pre-renal AKI from volume depletion. ATN characteristically shows a urine sodium greater than 40 mEq/L and dilute urine because tubular function is lost.

Correct. KDIGO AKI Stage 1 is defined as: serum creatinine rise of at least 0.3 mg/dL within 48 hours (here: 1.4 minus 0.9 = 0.5 mg/dL rise) OR 1.5 to 1.9 times baseline, OR urine output less than 0.5 mL/kg/h for 6 to 12 hours. This patient meets BOTH the creatinine criterion (rise of 0.5 mg/dL) and the urine output criterion (0.3 mL/kg/h for 12 hours), placing him in Stage 1 (whichever criterion is highest). For Stage 2, creatinine must reach 2 to 2.9 times baseline.

KDIGO AKI staging: Stage 1 = Cr rise at least 0.3 mg/dL in 48 h or 1.5-1.9x baseline, or UO less than 0.5 mL/kg/h for 6-12 h. Stage 2 = Cr 2-2.9x baseline or UO less than 0.5 mL/kg/h at least 12 h. Stage 3 = Cr 3x baseline, or Cr at least 4 mg/dL, or RRT initiated, or UO less than 0.3 mL/kg/h at least 24 h.

KDIGO AKI Stage 1: creatinine rise at least 0.3 mg/dL within 48 h or 1.5 to 1.9 times baseline, OR urine output less than 0.5 mL/kg/h for 6 to 12 h. Stage 2: creatinine 2 to 2.9 times baseline or UO less than 0.5 mL/kg/h for at least 12 h. Stage 3: creatinine 3 times baseline or rise to at least 4 mg/dL or UO less than 0.3 mL/kg/h for at least 24 h.

Correct. KDIGO GFR categories: G1 at least 90, G2 60-89, G3a 45-59, G3b 30-44, G4 15-29, G5 less than 15 mL/min/1.73 m2. An eGFR of 52 mL/min/1.73 m2 places her in G3a (45-59). Albuminuria categories: A1 less than 30 mg/g (normal to mildly increased), A2 30-300 mg/g (moderately increased), A3 greater than 300 mg/g (severely increased). ACR of 280 mg/g falls in A2 (30-300 mg/g). Therefore G3a/A2. The diagnosis requires persistence for 3 months — confirmed by two measurements 4 months apart.

KDIGO CKD GFR stages: G1 at least 90, G2 60-89, G3a 45-59, G3b 30-44, G4 15-29, G5 less than 15 mL/min/1.73m2. Albuminuria: A1 less than 30, A2 30-300, A3 greater than 300 mg/g (or mg/mmol equivalents). Both dimensions needed for prognosis. G3a/A2 = moderately high risk of progression.

KDIGO GFR categories: G3a = 45-59 mL/min/1.73 m2 (eGFR 52 falls here). Albuminuria categories: A1 less than 30 mg/g; A2 = 30-300 mg/g; A3 greater than 300 mg/g. ACR 280 mg/g falls in A2 (30-300 range). Correct staging is G3a/A2.

Correct. When hyperkalaemia causes ECG changes (peaked T waves, QRS widening, sine-wave pattern), the immediate priority is cardiac membrane stabilisation with intravenous calcium gluconate (10 mL of 10% over 2-3 minutes). Calcium does NOT lower potassium — it raises the threshold potential of myocardial cells, reducing the risk of fatal arrhythmia within 2-3 minutes. Potassium-lowering measures (insulin-dextrose, bicarbonate, salbutamol, kayexalate, dialysis) follow in parallel.

Hyperkalaemia ECG progression: peaked T waves → prolonged PR → widened QRS → sine-wave → VF. Step 1: IV calcium gluconate (cardiac membrane stabilisation, onset 2-3 min). Step 2: insulin 10 units + 50 mL 50% dextrose (shifts K+ intracellularly, lowers by 0.5-1 mEq/L). Step 3: sodium bicarbonate if acidosis. Step 4: kayexalate or patiromer (removes K+). Step 5: dialysis if refractory.

With ECG changes from hyperkalaemia, the first priority is cardiac membrane stabilisation with intravenous calcium gluconate — this does not lower potassium but protects the heart within 2-3 minutes by raising the threshold potential. Potassium-shifting agents (insulin-dextrose, bicarbonate) and removal strategies (kayexalate, dialysis) are added subsequently.

Correct. The AEIOU indications for emergency dialysis in AKI are: Acidosis (pH less than 7.1, refractory), Electrolytes (refractory hyperkalaemia greater than 6.5 mEq/L with ECG changes), Intoxication (dialysable toxins: methanol, ethylene glycol, lithium, salicylates), Overload (pulmonary oedema refractory to diuretics), Uraemia (encephalopathy, pericarditis, bleeding). This patient has both O (refractory pulmonary oedema) and A (pH 7.05, below the 7.1 threshold) — two absolute indications. The presence of even one AEIOU criterion is sufficient to initiate urgent dialysis.

AEIOU dialysis indications: Acidosis pH less than 7.1 (refractory), Electrolytes (K+ greater than 6.5 with ECG changes, Na less than 115 refractory), Intoxication (methanol, ethylene glycol, lithium, salicylates), Overload (pulmonary oedema refractory to diuretics), Uraemia (encephalopathy, pericarditis, uraemic bleeding). Any ONE criterion is sufficient.

The AEIOU indications for emergency dialysis: Acidosis (pH less than 7.1 refractory), Electrolytes (refractory hyperkalaemia with ECG changes), Intoxication (dialysable toxins), Overload (pulmonary oedema refractory to diuretics), Uraemia (encephalopathy, pericarditis). Creatinine level alone and oliguria alone are NOT absolute indications — the clinical consequences drive the decision.

Correct. Current guidance (BNF, KDIGO 2022) recommends: eGFR 45-59 (G3a): continue metformin with caution, review dose. eGFR 30-44 (G3b): reduce dose and review. eGFR less than 30 (G4-G5): STOP metformin (risk of lactic acidosis). This patient at eGFR 38 (G3b) should have her dose reduced, not stopped outright, and eGFR monitored every 3-6 months. Abrupt cessation is not necessary at G3b.

Metformin and CKD: safe at eGFR at least 45. Dose reduce at eGFR 30-44. STOP at eGFR less than 30. Also hold metformin temporarily if contrast media is used or if the patient is acutely unwell with risk of dehydration. Lactic acidosis (though rare) is the feared complication.

Metformin guidance by eGFR: eGFR at least 45 = continue; eGFR 30-44 = reduce dose and monitor; eGFR less than 30 = STOP (lactic acidosis risk). This patient has eGFR 38 (G3b) — dose reduction and 3-6 monthly monitoring is appropriate; abrupt cessation is not yet required.

Correct. The primary mechanism of anaemia in CKD is reduced erythropoietin (EPO) synthesis by the peritubular fibroblasts of the failing kidneys. EPO is the principal growth factor for erythroid precursors; its deficiency produces a normocytic, normochromic anaemia with a low reticulocyte count (hypoproliferative). Iron stores (ferritin 180, TSAT 22%) are within the functional range, excluding absolute iron deficiency as the primary cause.

Anaemia of CKD: normocytic, normochromic, hypoproliferative. Primary mechanism: reduced EPO synthesis by peritubular fibroblasts. Secondary contributors: functional iron deficiency, uraemic suppression of marrow, reduced RBC lifespan. Treat with ESAs (epoetin/darbepoetin) + IV iron to keep Hb 10-11.5 g/dL. Target Hb greater than 13 increases cardiovascular risk.

Anaemia of CKD is primarily caused by reduced erythropoietin (EPO) synthesis by the peritubular fibroblasts of the diseased kidneys. The result is a normocytic normochromic anaemia with low reticulocyte count. Treatment is erythropoiesis-stimulating agents (ESAs) plus IV iron if TSAT less than 20% or ferritin less than 200 ng/mL.

Correct. In CKD-MBD, the sequence is: reduced renal 1-alpha-hydroxylase → reduced 1,25-dihydroxyvitamin D3 → reduced intestinal calcium absorption → hypocalcaemia → persistent PTH stimulation → secondary hyperparathyroidism. Concurrent phosphate retention (eGFR falling) worsens the process by directly stimulating PTH secretion. The result is low calcium, high phosphorus, and markedly elevated PTH — the classic triad of secondary hyperparathyroidism in CKD.

CKD-MBD: reduced renal 1-alpha-hydroxylase → low 1,25-OH vitamin D3 → low Ca, high P, elevated FGF-23, high PTH (secondary hyperparathyroidism). Treat phosphate with binders (calcium carbonate, sevelamer) and vitamin D analogues (calcitriol/alfacalcidol). Cinacalcet for secondary hyperparathyroidism. Tertiary hyperparathyroidism = autonomous high-calcium secretion after prolonged secondary HPT.

CKD-MBD secondary hyperparathyroidism: reduced 1,25-OH vitamin D3 (from reduced renal 1-alpha-hydroxylase) → hypocalcaemia + phosphate retention → persistent PTH stimulation. Low calcium + high phosphorus + high PTH = secondary hyperparathyroidism. Primary hyperparathyroidism causes high calcium. Tertiary causes high calcium with autonomous secretion.

Correct. A fall in eGFR of up to 25-30% after starting an ACE inhibitor or ARB is expected and acceptable — it reflects the intended effect of reducing intraglomerular pressure (efferent arteriolar dilation), not true GFR loss. The drug should be continued if: eGFR fall is less than 25% from baseline, potassium is less than 5.5 mEq/L, and no bilateral renal artery stenosis is suspected. An eGFR fall of 25% (48 to 36) or potassium above 5.5 mEq/L would trigger withholding the drug. Here the fall is only about 12% — continue and monitor.

ACE inhibitors and ARBs are first-line for CKD proteinuria regardless of BP (especially diabetic nephropathy). An eGFR fall up to 25-30% at initiation is acceptable. Stop if fall greater than 30%, K+ greater than 5.5 mEq/L, or suspected bilateral renal artery stenosis. Never combine ACE inhibitor + ARB (dual blockade increases AKI and hyperkalaemia risk).

An eGFR fall of up to 25% after starting ACE inhibitor or ARB is expected and acceptable (reduced intraglomerular pressure via efferent vasodilation). Continue if eGFR fall less than 25%, K+ less than 5.5 mEq/L, and no bilateral RAS. This patient has only a 12% fall and K+ 5.3 — continue and monitor. Combined ACE+ARB dual blockade is NOT recommended (ONTARGET trial: increased harm).

Correct. Peritoneal dialysis (PD) uses the peritoneal membrane as the dialysis surface, can be performed at home (particularly CAPD and APD), avoids the need for vascular access (uses a Tenckhoff catheter), provides haemodynamic stability due to gradual solute removal, and consistently preserves residual renal function longer than haemodialysis. HD requires a functioning vascular access (AV fistula, graft, or tunnelled catheter) and is centre-based (typically 3 sessions per week, 4 hours each) for most patients.

Haemodialysis: vascular access (AV fistula preferred), centre-based 3-4 hours 3x/week, intermittent solute removal, cardiovascular instability risk. Peritoneal dialysis: Tenckhoff catheter, home-based, continuous or cyclic, gentler haemodynamics, better residual renal function preservation, risk of peritonitis. Renal transplant remains the gold standard for eligible patients.

PD uses the peritoneum as the dialysis membrane via a Tenckhoff catheter, can be done at home, is more haemodynamically stable, and better preserves residual renal function. HD requires AV fistula or catheter, is typically centre-based (3x/week), and produces larger haemodynamic shifts per session. Neither is universally superior — patient factors, social support, and clinical context guide the choice.