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

Inflammatory infiltration of the renal interstitium, most commonly caused by drug hypersensitivity (penicillins, NSAIDs, PPIs, rifampicin) or infection; classic triad of fever, rash, and eosinophilia present in <30% of cases; diagnosed by kidney biopsy.

Abrupt deterioration in renal function defined by KDIGO 2012 as serum creatinine rise ≥0.3 mg/dL within 48 h, ≥1.5× baseline within 7 days, or urine output <0.5 mL/kg/h for ≥6 consecutive hours.

The most common form of intrinsic AKI, caused by ischaemia (prolonged pre-renal state, septic shock) or nephrotoxins (aminoglycosides, contrast media, myoglobin); proximal tubular and thick ascending limb necrosis with granular and epithelial cell cast formation.

A process of discussion and documentation of a patient's wishes for future medical care in circumstances where they are unable to express preferences; legally recognised in India following the Common Cause vs Union of India Supreme Court ruling (2018); includes advance directives on dialysis continuation, CPR, and ventilatory support.

Mnemonic for emergency dialysis indications: Acidosis (metabolic, pH <7.1, refractory), Electrolytes (refractory hyperkalaemia), Intoxication (dialysable toxins), Overload (pulmonary oedema refractory to diuretics), Uraemia (pericarditis, encephalopathy, bleeding).

Spot urine test measuring urinary albumin normalised to urinary creatinine; preferred method for albuminuria quantification in CKD; first-morning sample preferred; <30 mg/g = A1, 30–300 = A2, >300 = A3.

KDIGO CKD albuminuria classification: A1 <30 mg/g ACR (normal to mildly increased), A2 30–300 mg/g (microalbuminuria), A3 >300 mg/g (macroalbuminuria/proteinuria).

Bedside test to confirm ulnar collateral circulation before radial artery puncture; both arteries occluded, hand blanched by fist pumping, ulnar artery released — normal = hand flushes within 5–10 seconds; confirms safety of radial artery sampling.

Calculated as serum [Na⁺] − ([Cl⁻] + [HCO₃⁻]); normal 8–12 mEq/L; elevated in high-AG metabolic acidosis (MUDPILES: Methanol, Uraemia, DKA, Propylene glycol, Isoniazid, Lactic acidosis, Ethanol toxic, Salicylates).

Urine output <100 mL/24 h; may indicate complete obstruction, severe ATN with anuria, or bilateral renal cortical necrosis; requires urgent investigation.

Surgically created connection between a peripheral artery and vein (usually radial artery + cephalic vein at the wrist) to provide high-flow vascular access for haemodialysis; gold standard permanent access; requires 3–6 months to mature and should be planned in CKD G4.

Flapping tremor elicited by dorsiflexion of the wrists, caused by brief lapses in postural tone from metabolic encephalopathy (uraemia, hepatic encephalopathy, CO₂ narcosis); a clinical sign of advanced uraemia.

The right of a capacitous adult patient to make informed decisions about their own medical care, including the right to refuse treatment; in ESRD, includes the right to refuse or withdraw dialysis.

The ethical obligation to act in the patient's best interest; in ESRD, requires presenting all modality options honestly and recommending the option most aligned with the patient's goals and values.

Legally recognised as death in India under THOA; certified by two independent physicians (not of the transplant team); allows organ donation after certification with next-of-kin consent.

Product of serum calcium (mg/dL) × serum phosphate (mg/dL); when >55 mg²/dL², risk of extraskeletal and vascular calcification increases significantly; mandates intensification of phosphate-lowering treatment in CKD.

Bidirectional functional deterioration of the heart and kidneys; Type 1 (acute): acute cardiac decompensation causing AKI (reduced cardiac output → renal hypoperfusion + RAAS activation); common in decompensated heart failure.

Abnormalities of kidney structure or function, present for >3 months, with implications for health; staged by the KDIGO system combining GFR categories G1–G5 and albuminuria categories A1–A3.

A calcimimetic agent that sensitises the calcium-sensing receptor on parathyroid cells to ambient calcium, suppressing PTH secretion; used in secondary hyperparathyroidism of dialysis patients; does not raise calcium or phosphate (unlike calcitriol).

Systemic disorder in CKD encompassing biochemical abnormalities (hyperphosphataemia, hypocalcaemia, elevated PTH and FGF-23, low calcitriol), bone disease (osteodystrophy), and vascular calcification.

Equation estimating creatinine clearance (GFR): [(140 − age) × weight] / (72 × creatinine) × 0.85 for females; preferred over CKD-EPI for drug dose adjustment purposes.

Management of ESRD without dialysis or transplantation; includes active treatment of all CKD complications (anaemia, hypertension, phosphate, acidosis) combined with palliative/symptom-focused care; an evidence-based option for elderly, frail, or multimorbid patients where dialysis provides limited survival benefit.

Slow continuous extracorporeal blood purification used in haemodynamically unstable ICU patients with AKI; avoids the rapid fluid shifts of intermittent haemodialysis; modalities include CVVH, CVVHD, and CVVHDF.

AKI occurring within 24–72 hours of iodinated contrast media administration; mechanism involves afferent arteriolar vasoconstriction (adenosine, endothelin) and direct tubulotoxicity; risk factors include pre-existing CKD, diabetes, and volume depletion.

The ability of a patient to understand information about their condition and treatment options, appreciate its relevance to their situation, reason about the options, and communicate a decision; may fluctuate in uraemic encephalopathy or dementia; formal assessment required if in doubt.

CKD caused by diabetic glomerulosclerosis, characterised by microalbuminuria progressing to macroalbuminuria, declining eGFR, and histological Kimmelstiel-Wilson nodules; the most common cause of ESRD worldwide.

Systematic review and modification of renally-cleared medications when AKI is identified; key drugs requiring adjustment: aminoglycosides (extend interval), vancomycin (monitor trough), digoxin (reduce dose), enoxaparin (reduce dose, monitor anti-Xa); drugs to stop: metformin, NSAIDs.

Estimated glomerular filtration rate calculated from serum creatinine, age, and sex using the CKD-EPI equation; the primary measure for CKD staging and monitoring; normal ≥90 mL/min/1.73 m².

Recombinant EPO preparations (erythropoietin-alpha, darbepoetin-alfa) used to treat anaemia of CKD; target Hb 10–11.5 g/dL; higher targets associated with increased cardiovascular events.

Glycoprotein hormone produced by peritubular fibroblasts in the renal cortex in response to hypoxia; stimulates erythroid progenitor proliferation; deficiency in CKD causes normocytic normochromic anaemia.

Osteocyte-derived hormone that rises early in CKD; promotes renal phosphaturia and suppresses 1α-hydroxylase (reducing calcitriol synthesis); elevated FGF-23 independently causes left ventricular hypertrophy.

The percentage of filtered sodium that is excreted in the urine; calculated as (urine Na × plasma creatinine) / (plasma Na × urine creatinine) × 100; <1% suggests pre-renal, >2% suggests ATN (unreliable in non-oliguric AKI or diuretic use).

Alternative to FENa in patients on diuretics; <35% = pre-renal AKI; urea reabsorption is not directly affected by loop or thiazide diuretics.

KDIGO CKD classification: G1 ≥90 (normal/high), G2 60–89 (mildly decreased), G3a 45–59, G3b 30–44, G4 15–29, G5 <15 mL/min/1.73 m² (kidney failure/ESRD).

Urinary protein loss resulting from disruption of the glomerular filtration barrier (podocyte injury, GBM damage); predominantly albuminuria; quantified by urine ACR; >300 mg/g = A3; >3.5 g/24 h = nephrotic-range.

Urinary casts composed of degenerated tubular epithelial cell debris; characteristic of acute tubular necrosis; presence confirms intrinsic tubular injury in AKI.

Urinary casts formed from degenerating tubular epithelial cells, characteristic of ATN; their presence on urine microscopy indicates tubular injury and distinguishes intrinsic AKI from pre-renal azotaemia.

Blood in the urine; glomerular haematuria produces dysmorphic red cells and RBC casts (suggesting GN); non-glomerular haematuria from calculi, tumour, or infection produces isomorphic red cells; detected on dipstick and confirmed by microscopy.

Acute-phase protein produced by the liver, elevated in CKD due to chronic inflammation; blocks intestinal iron absorption and iron release from macrophages, causing functional iron deficiency despite normal or elevated ferritin.

Dilatation of the renal pelvis and calyceal system due to obstruction to urine outflow; graded 1–4 on ultrasound; bilateral hydronephrosis in an anuric patient confirms post-renal AKI.

AKI caused by structural damage to the kidney parenchyma (tubules, glomeruli, interstitium, or vessels); the most common form is acute tubular necrosis (ATN).

The height of the venous blood column visible in the internal jugular vein with the patient at 45°; normally ≤3–4 cm above the sternal angle; elevated JVP indicates raised right atrial pressure, as in heart failure, fluid overload, or cardiac tamponade; flat JVP indicates hypovolaemia.

Fair allocation of healthcare resources; in ESRD, includes equitable access to dialysis and transplantation, prohibition on commercial organ trade, and allocation of deceased-donor organs by NOTTO/ZTCC criteria.

Kidney Disease: Improving Global Outcomes classification of AKI severity into Stage 1 (1.5–1.9× baseline creatinine or ≥0.3 mg/dL rise), Stage 2 (2.0–2.9×), and Stage 3 (≥3× or creatinine ≥4.0 mg/dL or initiation of RRT), with corresponding urine output thresholds.

Validated patient-reported outcome measure for CKD and dialysis patients; covers physical function, energy, sleep, social function, kidney disease burden, cognitive function, and overall health; used to monitor QoL trends and identify areas for intervention.

Deep, regular, sighing respirations representing respiratory compensation for metabolic acidosis; common in advanced AKI or CKD with significant acidaemia; named after Adolf Kussmaul.

Nail finding with distal brown/pink band and proximal white band; associated with hypoalbuminaemia and CKD; caused by oedema of the nail bed and melanin deposition.

A treatment is futile when it cannot achieve its intended physiological goal or when it can only prolong dying without meaningful improvement in quality of life; one of the ethical justifications for withholding or withdrawing treatment.

Administration of calcium gluconate 10% IV as the first step in life-threatening hyperkalaemia; acts within 1–3 minutes to antagonise the cardiac membrane effects of high potassium without affecting serum potassium levels.

Clinical syndrome of heavy proteinuria (>3.5 g/24 h in adults), hypoalbuminaemia, oedema, and hyperlipidaemia; causes effective intravascular volume depletion despite total body fluid excess, resulting in pre-renal AKI.

A substance that causes direct or indirect damage to renal tubular cells; common examples include aminoglycosides, NSAIDs, iodinated contrast media, cisplatin, amphotericin B, myoglobin, and certain traditional herbal preparations.

The ethical obligation to avoid harm; in ESRD, includes the concept of medical futility — not initiating or continuing treatments that prolong dying without meaningful benefit.

Acute tubular necrosis in which urine output remains ≥400 mL/24 h despite elevated creatinine; seen most commonly with aminoglycoside nephrotoxicity; generally associated with a better prognosis than oliguric ATN.

National body coordinating deceased-donor organ allocation in India; maintains the national waitlist; allocates organs based on compatibility, urgency, and time on waitlist; regional ZTCCs implement local allocation.

Urine output <0.5 mL/kg/h or <400 mL/24 h in adults; a cardinal sign of significant AKI, reflecting the kidney's inability to maintain adequate filtration or indicating physiological conservation response.

The earliest ECG sign of hyperkalaemia; narrow-based, tall, symmetric T-waves (tent-shaped), best seen in V2–V4; caused by accelerated repolarisation from elevated extracellular K⁺; typically appears at K⁺ 5.5–6.0 mEq/L.

RRT using the peritoneum as a dialysis membrane; dialysate instilled into the peritoneal cavity via a permanent catheter; CAPD = 4 manual exchanges/day; APD = overnight automated exchanges; preferred in haemodynamically stable patients, children, and those without suitable vascular access.

Medications taken with meals to bind dietary phosphate in the GI tract and reduce absorption; calcium carbonate (limit total Ca to <1.5 g elemental/day), sevelamer carbonate (preferred with vascular calcification), or lanthanum carbonate; must be taken WITH food, not after.

Oedema characterised by a persistent pit after pressure release; graded 1–4 by depth of pit and extent up the limb; in renal failure indicates volume overload, hypoalbuminaemia (nephrotic syndrome), or heart failure.

Brisk polyuria (often >3–4 L/day) occurring after relief of prolonged urinary obstruction; caused by osmotic diuresis from accumulated urea and tubular immaturity; requires careful fluid replacement to prevent severe volume and electrolyte depletion.

AKI caused by obstruction to urine outflow at any level from the collecting system to the urethra; diagnosed by hydronephrosis on ultrasound; treated by relieving the obstruction.

A fall in systolic BP >20 mmHg or diastolic BP >10 mmHg on standing from a supine position; a reliable clinical indicator of intravascular volume depletion in the context of AKI evaluation.

Referral to a transplant centre for kidney transplantation evaluation when eGFR reaches approximately 20 mL/min/1.73 m², before dialysis is initiated; associated with superior outcomes compared to transplantation after dialysis.

AKI caused by inadequate renal perfusion with structurally intact nephrons; urine is concentrated (FENa <1%, urine osmolality >500 mOsm/kg); reversible with restoration of perfusion.

Neurohumoral axis activated in CKD causing hypertension via angiotensin II-mediated vasoconstriction and aldosterone-mediated sodium retention; ACE inhibitors and ARBs block this axis to lower BP, reduce proteinuria, and slow CKD progression.

Use of ACE inhibitors or ARBs to reduce intraglomerular pressure and proteinuria in CKD; first-line antihypertensives in CKD with proteinuria; dual RAAS blockade (ACE+ARB) is contraindicated; a creatinine rise ≤30% and K⁺ ≤5.5 after initiation is acceptable.

A clinical syndrome of rapidly declining renal function (GFR falling by ≥50% within weeks) due to severe glomerular injury, typically crescentic GN; requires urgent biopsy and immunosuppression to prevent permanent dialysis.

Urinary casts formed when red blood cells cross the damaged glomerular filtration barrier and are moulded in the tubule; pathognomonic of glomerulonephritis; require urgent immunological workup and potential renal biopsy.

Structured nutritional guidance for CKD/AKI patients covering protein (0.8–1.0 g/kg/day in non-dialysis AKI, 1.2–1.5 in dialysis), potassium restriction (avoid high-K foods, boil vegetables), phosphate restriction (limit dairy, processed food with phosphate additives + binders with meals), sodium <2 g/day, and fluid restriction.

Mechanical filtration of blood used when the kidneys can no longer maintain homeostasis; modalities include intermittent haemodialysis (IHD) and continuous renal replacement therapy (CRRT); indicated by the AEIOU criteria in AKI.

Breakdown of skeletal muscle releasing myoglobin into the circulation; myoglobin causes AKI through tubular obstruction by ferrihemate casts, direct oxidative tubular injury, and afferent arteriolar vasoconstriction; characterised by dark (cola-coloured) urine and elevated serum creatine kinase.

Yellowish-brown skin discolouration in advanced CKD caused by accumulation of retained carotenoid-like uraemic pigments; distinct from jaundice (which also involves sclera) and contributes to the characteristic appearance of long-standing uraemia.

Chronically elevated PTH driven by low calcitriol, hypocalcaemia, and hyperphosphataemia in CKD; leads to osteitis fibrosa cystica and vascular calcification; managed with phosphate binders, calcitriol analogues, and cinacalcet.

Sodium-glucose cotransporter-2 inhibitors (empagliflozin, dapagliflozin, canagliflozin) that reduce intraglomerular pressure by natriuresis-mediated tubuloglomerular feedback; shown in CREDENCE, DAPA-CKD, and EMPA-KIDNEY trials to reduce ESRD risk.

Pre-terminal ECG pattern in severe hyperkalaemia (K⁺ >7.5 mEq/L) in which widened QRS merges with peaked T-wave creating a smooth biphasic wave; indicates impending ventricular fibrillation; requires immediate calcium gluconate.

A person who makes healthcare decisions for a patient who lacks decision-making capacity; typically the nearest relative in Indian clinical practice; should ideally use substituted judgement (what would the patient have wanted?) rather than the surrogate's own preferences.

Indian legislation (1994, amended 2011) governing organ donation and transplantation; permits living-related donation (hospital medical board approval), living-unrelated donation (Authorisation Committee), and deceased-donor donation after brain stem death; criminalises commercial organ dealing.

The clinical syndrome resulting from accumulation of nitrogenous waste products and loss of renal endocrine and regulatory functions in advanced CKD; manifests with GI, neurological, cardiovascular, haematological, and dermatological complications.

White crystalline deposits on the skin from urea precipitation through sweat; pathognomonic of severe uraemia; rarely seen in current practice given earlier initiation of dialysis.

Fibrinous pericarditis caused by uraemic toxin-induced pericardial inflammation in advanced CKD; presents with pleuritic chest pain, pericardial rub, and ECG changes; an indication for urgent dialysis.

Impaired platelet aggregation and thromboxane A₂ production caused by retained uraemic toxins; results in bleeding tendency (prolonged bleeding time) despite normal platelet count; corrected by dialysis, DDAVP, or conjugated oestrogens.

Serum urea (mg/dL) divided by serum creatinine (mg/dL); ratio >20 suggests pre-renal AKI (increased tubular urea reabsorption) or gastrointestinal haemorrhage; ratio <10 suggests intrinsic renal disease or low protein intake.

Predicts expected PaCO₂ for respiratory compensation in pure metabolic acidosis: expected PaCO₂ = (1.5 × HCO₃⁻) + 8 ± 2 mmHg; if measured PaCO₂ is higher, superimposed respiratory acidosis is present.

Regional bodies under NOTTO that coordinate deceased-donor organ procurement and allocation within their zone; manage the regional waitlist and coordinate with hospitals certified for transplantation.