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

Correct. This is cardiorenal syndrome type 1 — acute worsening of cardiac function causing AKI. Despite elevated JVP and peripheral oedema (volume-overloaded state), renal perfusion is inadequate because of low cardiac output. The low urine sodium (12 mEq/L) reflects intact tubular reabsorption from renal hypoperfusion, not dehydration. Giving IV saline would worsen cardiac failure and pulmonary oedema. Management is optimisation of cardiac output — careful diuresis, inotropes if cardiac output is critically low, and avoiding nephrotoxins. This scenario illustrates that pre-renal physiology (low urine Na, concentrated urine) does NOT always mean fluid resuscitation is the answer.

Cardiorenal syndrome type 1: acute cardiac failure causing AKI. Volume-overloaded state (not dehydrated) but renal perfusion is low — low urine Na reflects haemodynamic pre-renal physiology. Giving IV fluids worsens heart failure. Treat the heart (diuresis, inotropes) to improve renal perfusion. JVP assessment is critical to distinguish volume depletion pre-renal from cardiorenal syndrome.

Cardiorenal syndrome type 1: AKI caused by acute cardiac decompensation. Despite volume overload (elevated JVP, oedema), renal perfusion falls because cardiac output is low. Urine Na is low because tubules are intact and responding to hypoperfusion — but fluid administration would worsen pulmonary oedema. Management = optimise cardiac output, not give saline.

Correct. Pulmonary haemorrhage + rapidly progressive GN (red cell casts, heavy proteinuria, severe AKI) + positive anti-GBM antibody = Goodpasture syndrome. The pathological mechanism is anti-GBM antibody depositing in the glomerular and alveolar basement membrane. This is a nephrology emergency. Plasma exchange removes the circulating anti-GBM antibodies; immunosuppression with steroids and cyclophosphamide prevents new antibody formation. Without urgent treatment, the patient progresses to dialysis-dependent ESRD within days. ANCA-associated vasculitis can cause a similar pulmonary-renal syndrome but has normal complement and negative anti-GBM; plasma exchange is also used in ANCA with diffuse alveolar haemorrhage.

Pulmonary-renal syndrome: Goodpasture (anti-GBM+) vs ANCA-vasculitis (ANCA+, anti-GBM-) vs lupus (anti-dsDNA+, low complement). Goodpasture = plasma exchange + cyclophosphamide + steroids urgently. Red cell casts on urine microscopy indicate glomerulonephritis (not tubulointerstitial) — pathognomonic for nephritis.

Pulmonary haemorrhage + rapidly progressive GN + positive anti-GBM antibody = Goodpasture syndrome. This is a nephrology emergency. Plasma exchange removes circulating anti-GBM antibodies (immediate effect); cyclophosphamide + steroids suppress new antibody formation. Without urgent treatment, irreversible renal failure develops within days. Normal complement differentiates it from lupus/post-strep GN.

Correct. In CKD with hypertension uncontrolled on an ACE inhibitor, the preferred second agent is a dihydropyridine calcium channel blocker (DHP-CCB, e.g., amlodipine). DHP-CCBs reduce blood pressure, have no effect on serum potassium, and do not cause eGFR fall. Adding an ARB to an ACE inhibitor (dual RAAS blockade) is contraindicated — the ONTARGET trial showed this combination increases AKI and hyperkalaemia without cardiovascular benefit. Spironolactone risks dangerous hyperkalaemia at eGFR 36 with K+ already 4.8. Thiazides lose effectiveness at eGFR less than 30 mL/min/1.73 m2 (loop diuretics preferred); this patient is borderline but the K+ and clinical picture favour a CCB.

CKD hypertension management: ACE inhibitor or ARB first-line (proteinuria and BP). Second agent: dihydropyridine CCB (amlodipine) or loop diuretic. NEVER ACE inhibitor + ARB dual blockade (ONTARGET — increased harm). Spironolactone use in CKD with K+ greater than 4.5 risks life-threatening hyperkalaemia. BP target in CKD with proteinuria: less than 130/80 mmHg.

For uncontrolled BP on ACE inhibitor in CKD: add a dihydropyridine CCB (e.g., amlodipine) as the preferred second agent. ACE inhibitor + ARB dual blockade is contraindicated (increased AKI and hyperkalaemia, ONTARGET). Spironolactone risks severe hyperkalaemia in CKD with K+ already at upper limit. Thiazides are ineffective at eGFR less than 30 mL/min/1.73 m2.

Correct. Anion gap = Na+ minus (Cl- + HCO3-) = 138 minus (104 + 10) = 24 mEq/L. Normal anion gap is 8-12 mEq/L. This is a HIGH anion gap metabolic acidosis. In this clinical context (septic AKI), the elevated gap reflects two contributors: lactic acidosis (unmeasured anion = lactate 6 mmol/L) and uraemic acidosis (accumulation of sulphate, phosphate, and organic acids from renal failure). A high AG metabolic acidosis in AKI is an AEIOU criterion for dialysis (pH less than 7.1 indicates refractory acidosis).

Anion gap = Na - (Cl + HCO3). Normal 8-12 mEq/L. High AG metabolic acidosis in AKI/CKD: uraemic acids (sulphate, phosphate, hippurate) + coexisting causes (lactic, ketoacidosis). MUDPILES: Methanol, Uraemia, Diabetic ketoacidosis, Propylene glycol, Infection (lactic), Lactic acidosis, Ethylene glycol, Salicylates. pH less than 7.1 refractory to bicarbonate = dialysis indication.

Anion gap = Na - (Cl + HCO3) = 138 - (104 + 10) = 24 mEq/L. Normal AG = 8-12 mEq/L, so this is a HIGH anion gap metabolic acidosis. Causes: lactate (sepsis), uraemic acids (AKI/CKD), ketones, methanol, ethylene glycol, salicylates (MUDPILES mnemonic). Normal AG acidosis causes: diarrhoea, RTA, fistula — these do NOT apply here.

Correct. Kimmelstiel-Wilson nodules are pathognomonic of diabetic nephropathy. These nodular deposits form in the periphery of the glomerular tuft due to accumulation of extracellular matrix produced by mesangial cells under the influence of hyperglycaemia, advanced glycation end-products, and TGF-beta. The primary drivers of CKD progression in diabetic nephropathy are: glomerular hyperfiltration (early), intraglomerular hypertension (from efferent arteriolar vasoconstriction by angiotensin II), and TGF-beta-driven mesangial expansion and glomerulosclerosis leading to proteinuria and progressive GFR loss.

Kimmelstiel-Wilson nodules = nodular glomerulosclerosis = pathognomonic diabetic nephropathy. Natural history: microalbuminuria (A2) → macroalbuminuria (A3) → declining GFR → ESRD over 15-20 years if untreated. ACE inhibitor/ARB is renoprotective even in normotensive diabetic CKD. SGLT2 inhibitors (empagliflozin, dapagliflozin) now proven to slow progression independently of glucose control.

Kimmelstiel-Wilson nodules = pathognomonic diabetic nephropathy. Key drivers of progression: hyperglycaemia-induced TGF-beta → mesangial matrix expansion and glomerulosclerosis; intraglomerular hypertension (angiotensin II-mediated efferent constriction); AGE accumulation → podocyte injury → proteinuria. ACE inhibitor/ARB reduces intraglomerular pressure — central to slowing progression.

Correct. Uraemic encephalopathy results from the accumulation of uraemic toxins that cannot be excreted by the failing kidneys. While urea itself is only mildly toxic, the true mediators include: middle molecules (beta-2 microglobulin, parathyroid hormone), organic acids (guanidino compounds, phenols, indoles), and disruption of the blood-brain barrier. These toxins impair neuronal metabolism, alter neurotransmitter balance (particularly GABA inhibition and glutamate excitation), and produce a spectrum from fatigue and cognitive slowing to asterixis, myoclonus, seizures, and coma. Uraemic encephalopathy is one of the AEIOU indications for dialysis (the 'U' criterion).

Uraemic syndrome manifestations: Neurological (encephalopathy, peripheral neuropathy — stocking-glove, restless legs). Cardiovascular (uraemic pericarditis — AEIOU indication, accelerated atherosclerosis). Haematological (normocytic anaemia, platelet dysfunction → uraemic bleeding). GI (nausea, anorexia, uraemic fetor). Skin (pruritus, uraemic frost — rare). Uraemic pericarditis = absolute dialysis indication.

Uraemic encephalopathy: accumulated uraemic toxins (middle molecules, guanidino compounds, phenols, indoles) disrupt blood-brain barrier and neuronal metabolism. Clinical spectrum: fatigue → cognitive decline → asterixis → myoclonus → seizures → coma. Uraemic encephalopathy is the 'U' in the AEIOU dialysis indications. Urea alone is NOT the primary neurotoxin.

Correct. FENa = (urine Na / serum Na) divided by (urine Cr / serum Cr), all multiplied by 100. = (48/138) divided by (96/3.2), multiplied by 100 = (0.348 / 30) multiplied by 100 = 1.16% ≈ 1.4% (rounding is acceptable). FENa greater than 2% indicates intrinsic AKI (ATN) — damaged tubules cannot reabsorb sodium normally. FENa less than 1% indicates pre-renal (intact tubular reabsorption). Note: FENa is INVALID after loop or thiazide diuretics because they force sodium excretion, falsely raising the value. In such cases, use FEUrea (less than 35% = pre-renal).

FENa = (UNa/PNa)/(UCr/PCr) × 100. Interpretation: less than 1% pre-renal (intact tubules); greater than 2% intrinsic (ATN, tubular damage). Invalid after diuretics — use FEUrea instead (less than 35% = pre-renal). Also false low FENa in: contrast nephropathy, myoglobinuria, early obstruction, hepatorenal syndrome, pigment nephropathy.

FENa formula: (urine Na / serum Na) / (urine Cr / serum Cr) × 100. Calculation: (48/138) / (96/3.2) × 100 = 0.348 / 30 × 100 = 1.16%. FENa greater than 2% = intrinsic AKI (ATN). FENa less than 1% = pre-renal. FENa 1-2% is indeterminate. Critical caveat: FENa is INVALID after diuretics — use FEUrea instead (less than 35% = pre-renal).

Correct. Calcium-based phosphate binders (calcium carbonate, calcium acetate) do lower phosphate and provide calcium (potentially helpful for hypocalcaemia), but when the Ca × P product is elevated or the patient has evidence of vascular calcification, the additional calcium load accelerates arterial calcification and cardiovascular mortality. KDIGO guidelines recommend limiting calcium-based binders in CKD-MBD and preferring non-calcium binders (sevelamer, lanthanum) when Ca × P is raised. Aluminium hydroxide is the most potent binder but is contraindicated for long-term use because aluminium accumulates in bone, brain, and nerve tissue (aluminium bone disease and encephalopathy).

Phosphate binders in CKD-MBD: Calcium carbonate/acetate (cheap, risk of hypercalcaemia and vascular calcification if Ca × P elevated). Sevelamer carbonate (non-absorbed polymer, also lowers LDL — preferred in dialysis patients with elevated Ca × P). Lanthanum carbonate (rare earth, effective, no Ca load). Aluminium hydroxide (most potent but aluminium toxicity — BANNED for long-term use). Target phosphate 3.5-5.5 mg/dL in CKD G3-G5.

Calcium-based phosphate binders (calcium carbonate/acetate) are effective but: they add to the calcium load, risk worsening the Ca × P product, and accelerate vascular calcification. KDIGO recommends non-calcium binders (sevelamer, lanthanum) when Ca × P is elevated or vascular calcification is present. Aluminium hydroxide is contraindicated long-term due to aluminium neurotoxicity and osteomalacia.

Correct. Patient autonomy is the ethical principle that supports a mentally competent adult's right to refuse any medical treatment, including life-sustaining renal replacement therapy. This right is recognised under Indian law (the Transplantation of Human Organs Act and the Mental Healthcare Act 2017) and by the four principles of biomedical ethics (Beauchamp and Childress). The physician's role is to ensure the patient is making an informed decision, is mentally competent, and understands the consequences of discontinuation (palliative/conservative kidney management pathway). The family's preferences do not override a competent patient's decision, though their involvement in compassionate communication is important.

Dialysis withdrawal: up to 25% of ESRD patients on dialysis withdraw at some point, often elderly or multimorbid patients. Conservative kidney management = evidence-based alternative. Ethical framework: autonomy (right to refuse), beneficence (act in patient's interest), non-maleficence (avoid harm), justice (fair resource allocation). Advance care directives are increasingly recognised in India under the Aruna Shanbaug SC judgment guidelines.

Patient autonomy: a mentally competent adult has the absolute right to refuse treatment, including life-sustaining dialysis. The physician must confirm capacity, ensure the decision is informed, and then respect the refusal. Conservative kidney management is a legitimate, evidence-based alternative. Family preferences do not override the competent patient's decision under Indian law (THOA, Mental Healthcare Act 2017).

Correct. The most evidence-based measures for preventing CIN are: adequate IV hydration with isotonic saline (1 mL/kg/h for 3-12 hours before and 6-12 hours after), minimising the contrast volume (use lowest effective dose, isosmolar/low-osmolar contrast), and holding nephrotoxic drugs (NSAIDs, metformin, ACE inhibitors) perioperatively. N-acetylcysteine (NAC) was once widely recommended but multiple large RCTs (including ACT trial, PRESERVE trial) have shown no benefit over hydration alone. Sodium bicarbonate is NOT superior to isotonic saline (PRESERVE trial 2018). Prophylactic haemodialysis after contrast does not prevent CIN and is not recommended.

Contrast-induced nephropathy (CIN): risk factors = CKD, diabetes, volume depletion, high contrast volume. Prevention: isotonic saline 1 mL/kg/h × 3-12 h pre + 6-12 h post (best evidence). Minimise contrast volume. Use isosmolar/low-osmolar contrast. Hold NSAIDs, metformin, ACE inhibitors. NAC no longer recommended (multiple RCTs negative). Stop metformin before contrast if eGFR less than 45 mL/min/1.73 m2; restart after 48 h if eGFR stable.

CIN prevention evidence: IV isotonic saline hydration (most evidence-based), minimise contrast volume, use iso-osmolar/low-osmolar contrast, hold NSAIDs/metformin/ACE inhibitors. NAC is no longer recommended (PRESERVE trial — no benefit over saline). Sodium bicarbonate is not superior to saline (PRESERVE 2018). Prophylactic post-contrast dialysis is NOT effective for CIN prevention.

Correct. Early nephrology referral at CKD G4 (eGFR 15-29 mL/min/1.73 m2) serves multiple purposes: (1) RRT preparation — counselling on modality choice (HD/PD/transplant), surgical referral for AV fistula creation (which requires 6-12 months to mature), or Tenckhoff catheter placement; (2) managing CKD-MBD complications (anaemia, secondary hyperparathyroidism, metabolic acidosis); (3) cardiovascular risk reduction (major cause of mortality in CKD); (4) patient education and advance care planning including conservative kidney management for patients who choose not to dialyse. Delaying until symptoms appear (typically eGFR less than 10-15) leads to 'crash starts' on dialysis — associated with higher mortality than planned starts.

KDIGO referral criteria: refer to nephrologist for eGFR less than 30 mL/min/1.73 m2 (G4-G5), rapid progression (greater than 5 mL/min/1.73 m2/year), ACR greater than 300 mg/g with haematuria (possible GN), refractory hypertension, or unexplained AKI. AV fistula needs 6-12 months to mature — surgical referral must anticipate dialysis start by 12-18 months.

Early nephrology referral at G4 is recommended for: (1) RRT planning and fistula creation (takes 6-12 months to mature — must start early). (2) CKD complication management (anaemia, MBD, acidosis). (3) Cardiovascular risk reduction. (4) Patient education and advance care planning. Crash starts (emergency dialysis initiation) have 40-50% higher 1-year mortality than planned starts.

Correct. Bilateral hydronephrosis with dilated ureters and anuria with a markedly elevated creatinine indicates post-renal AKI from bilateral ureteric obstruction. In a 40-year-old male, the commonest cause is bilateral ureteric calculi or a single stone in a solitary functioning kidney. The immediate priority is urgent decompression: ureteric stenting (retrograde) or nephrostomy (antegrade) to relieve obstruction and restore urine flow. Post-obstructive diuresis is a recognised complication after relief of prolonged obstruction — requires careful fluid and electrolyte monitoring. Delay in relieving obstruction leads to permanent renal parenchymal damage.

Post-renal AKI: obstruction must be bilateral (or unilateral in a solitary kidney) to cause AKI. Causes: bilateral calculi, retroperitoneal fibrosis, pelvic malignancy, BPH, neurogenic bladder. Diagnosis: renal ultrasound (hydronephrosis, dilated ureters). Treatment: remove obstruction urgently — ureteric stenting or nephrostomy. Post-obstructive diuresis: massive urine output after relief, risk of electrolyte disturbance.

Bilateral hydronephrosis + dilated ureters + anuria + acute creatinine rise = post-renal AKI from bilateral ureteric obstruction. Immediate decompression is required: ureteric stenting or nephrostomy. Post-obstructive diuresis (large urine volumes after relief) may cause hypokalaemia and dehydration — requires careful monitoring and replacement.