CAQ-Nephrology key terms

A clinical constellation of heavy proteinuria (typically >3.5 g/day), hypoalbuminemia, edema, and hyperlipidemia resulting from increased glomerular permeability to plasma proteins.

A syndrome of hematuria with dysmorphic red cells or red cell casts, hypertension, oliguria, and variable proteinuria caused by glomerular inflammation and capillary injury.

A podocyte disorder causing abrupt nephrotic syndrome, usually with normal light microscopy and foot-process effacement on electron microscopy; steroid-responsive in most children and many adults.

Glomerular scarring affecting some glomeruli (focal) and part of each tuft (segmental), producing nephrotic-range proteinuria and often progressing to chronic kidney disease.

An autoimmune glomerulopathy with subepithelial immune deposits and thickened capillary loops, causing nephrotic syndrome in adults; associated with anti-PLA2R antibodies in primary cases.

The most common primary glomerulonephritis, marked by IgA-dominant mesangial deposits and episodic gross hematuria or persistent microscopic hematuria, often after mucosal infection.

Autoantibodies against the glomerular basement membrane cause rapidly progressive glomerulonephritis; lung hemorrhage with renal failure is called Goodpasture syndrome.

Small-vessel vasculitis with antineutrophil cytoplasmic antibodies, causing pauci-immune crescentic glomerulonephritis plus respiratory or systemic features; examples include granulomatosis with polyangiitis and microscopic polyangiitis.

Severe glomerular injury with extracapillary proliferation forming crescents in Bowman space, presenting as rapidly progressive renal failure and often hematuria with red cell casts.

Inflammation of renal tubules and interstitium, commonly drug-induced, causing acute kidney injury with sterile pyuria, white cell casts, and impaired concentrating ability.

Serum sodium below the normal range, usually reflecting water excess relative to solute; symptoms range from nausea to seizures and depend on severity and rate of onset.

Central pontine and extrapontine myelinolysis caused by overly rapid correction of chronic hyponatremia, producing dysarthria, quadriparesis, locked-in state, or death.

Syndrome of inappropriate antidiuretic hormone secretion: euvolemic hypotonic hyponatremia with concentrated urine and high urine sodium, caused by tumors, lung disease, or central nervous system disorders.

Elevated serum potassium that can cause life-threatening cardiac arrhythmias; common triggers include kidney failure, drugs, acidosis, and cell lysis.

Metabolic acidosis with elevated anion gap from accumulation of unmeasured acids such as lactate, ketones, uremic toxins, or toxins (methanol, ethylene glycol, salicylate).

Disorders of renal acid excretion causing hyperchloremic metabolic acidosis; types include distal (type 1), proximal (type 2), and hyperkalemic (type 4).

A calculation (urine Na + K − Cl) used to estimate urinary ammonium excretion; a positive value suggests impaired acid excretion in hyperkalemic or distal renal tubular acidosis.

The percentage of filtered sodium excreted, calculated from serum and urine sodium and creatinine; low values often indicate prerenal states, but diuretics and intrinsic disease reduce reliability.

Deficient antidiuretic hormone secretion (central) or renal resistance to it (nephrogenic), causing hypotonic polyuria, hypernatremia, and intense thirst.

An abrupt decline in kidney function defined by a rise in serum creatinine or fall in urine output over hours to days, staged by KDIGO criteria.

Kidney hypoperfusion from volume depletion, low cardiac output, or vasodilation that reverses with restoring perfusion; urine sodium is typically low and concentrating ability preserved.

Intrinsic kidney injury from ischemia or nephrotoxins causing tubular cell damage, muddy brown casts, and prolonged AKI; often requires supportive care and dialysis in severe cases.

Functional kidney failure in advanced liver disease from splanchnic vasodilation and renal vasoconstriction, diagnosed after excluding other causes and often treated with vasoconstrictors plus albumin.

Acute kidney injury occurring after iodinated contrast exposure, typically transient and diagnosed when other causes are excluded; risk is highest with preexisting kidney disease and volume depletion.

Muscle breakdown releasing myoglobin and intracellular contents, causing pigment nephropathy, hyperkalemia, hyperphosphatemia, and hypocalcemia; aggressive fluids are mainstays of prevention.

Slow, continuous extracorporeal dialysis used in hemodynamically unstable patients with severe acute kidney injury; it allows gradual fluid removal and avoids large osmotic shifts.

Kidney damage or reduced glomerular filtration rate persisting at least three months, staged by GFR category and albuminuria to guide treatment and prognosis.

A systemic disorder of mineral metabolism in chronic kidney disease with abnormal calcium, phosphate, parathyroid hormone, and vitamin D, causing vascular calcification and bone disease.

Measured by urea clearance relative to distribution volume (Kt/V) and by urea reduction ratio; target values reflect sufficient small-solute clearance and are linked to better outcomes.

Home dialysis using the peritoneal membrane as a filter, with dextrose-based solutions exchanged through a catheter; it preserves residual kidney function but risks peritonitis and membrane failure.

A surgically created connection between an artery and vein, usually in the forearm, that provides high-flow vascular access for hemodialysis; maturation takes weeks to months.

Kidney transplant rejection driven by donor-specific antibodies against graft antigens, with capillary inflammation and C4d deposition; treated with plasmapheresis and immunosuppression.

T-cell-mediated transplant rejection with interstitial inflammation and tubulitis, often presenting as rising creatinine; diagnosed by biopsy and treated with corticosteroids and immunosuppression adjustment.

Hypertension caused by renal artery stenosis, often from atherosclerosis or fibromuscular dysplasia; clues include refractory hypertension, flash pulmonary edema, or worsening function after ACE inhibitor.

Noninflammatory arterial disease causing string-of-beads narrowing in renal arteries of young women, leading to renovascular hypertension; angioplasty is often effective.

Ostial renal artery narrowing from atherosclerosis in older patients with vascular risk factors, contributing to hypertension and ischemic nephropathy; revascularization benefits are limited.

Abrupt severe hypertension with acute kidney injury and microangiopathic hemolysis in systemic sclerosis, treated urgently with ACE inhibitors; often with oliguria and hypertensive encephalopathy.

Small-vessel thrombosis with schistocytes, thrombocytopenia, and organ injury, seen in TTP, HUS, atypical HUS, and scleroderma renal crisis; kidney biopsy shows endothelial swelling and thrombi.

Pregnancy disorder after 20 weeks with new hypertension and proteinuria or organ dysfunction, including renal injury; delivery is definitive, and postpartum persistence suggests other disease.

Chronic kidney damage from diabetes with albuminuria and declining GFR, often accompanied by retinopathy; treatment targets glucose, blood pressure, and renin-angiotensin blockade.