ABIM Nephrology key terms

A clinical pattern of glomerular inflammation marked by hematuria with red cell casts, variable proteinuria, hypertension, edema, and declining kidney function, reflecting injury to the glomerular capillary wall and filtration barrier.

A glomerular disorder defined by heavy proteinuria (typically over 3.5 g per day), hypoalbuminemia, edema, hyperlipidemia, and lipiduria, resulting from increased permeability of the glomerular filtration barrier to plasma proteins.

A cylindrical structure formed in renal tubules from precipitated protein matrix trapping red blood cells, indicating glomerular bleeding; its presence in urine sediment strongly suggests active glomerulonephritis rather than lower urinary tract bleeding.

Rapidly progressive glomerular injury in which proliferating epithelial cells and macrophages fill Bowman space, compressing the capillary tuft; untreated it causes irreversible loss of kidney function within weeks.

A necrotizing crescentic glomerulonephritis with little or no immunoglobulin deposition on immunofluorescence, most often caused by antineutrophil cytoplasmic antibodies associated with small-vessel vasculitis.

Autoimmune disease in which antibodies target the noncollagenous domain of type IV collagen in glomerular and alveolar basement membranes, causing rapidly progressive glomerulonephritis, with or without pulmonary hemorrhage (Goodpasture syndrome).

A pattern on kidney biopsy immunofluorescence in which immunoglobulin deposits trace smoothly along glomerular capillary walls, characteristic of anti-glomerular basement membrane disease and contrasting with granular immune-complex deposition.

A biopsy immunofluorescence pattern of lumpy, discontinuous immunoglobulin and complement deposits along capillary walls or in mesangium, typical of immune-complex glomerulonephritis such as lupus nephritis or postinfectious glomerulonephritis.

A nephrotic glomerulopathy with normal glomeruli by light microscopy and diffuse foot process effacement on electron microscopy, most common in children and often steroid-responsive; it may be triggered by nonsteroidal anti-inflammatory drugs.

A glomerular lesion in which some glomeruli show sclerosis of part of the tuft, causing nephrotic-range proteinuria; it may be primary, adaptive, or genetic and frequently recurs after kidney transplantation.

A nephrotic glomerulopathy featuring subepithelial immune deposits and thickened capillary walls; most adult cases are primary and associated with antibodies to the phospholipase A2 receptor.

An autoantibody against the M-type phospholipase A2 receptor on podocytes, detectable in the majority of primary membranous nephropathy cases and useful for diagnosis and monitoring disease activity.

The most common primary glomerulonephritis worldwide, caused by IgA-containing immune complexes in the mesangium; it presents with episodic gross hematuria during mucosal infections or with slowly progressive proteinuric disease.

Immune complexes or other material localized in the mesangium between glomerular capillary loops, visualized by immunofluorescence or electron microscopy; dominant IgA deposition defines IgA nephropathy.

Immune-complex glomerulonephritis caused by systemic lupus erythematosus, classified by biopsy into proliferative, membranous, and other patterns; proliferative forms require immunosuppression to prevent progression to kidney failure.

Retraction and spreading of podocyte foot processes along the glomerular basement membrane, reducing filtration slit integrity and producing proteinuria; seen on electron microscopy in many proteinuric diseases.

Autoantibodies directed against neutrophil granule proteins, chiefly proteinase-3 and myeloperoxidase, that activate neutrophils and small vessels; they are serologic markers of pauci-immune vasculitis and glomerulonephritis.

Reversible injury to tubular epithelial cells from ischemia or nephrotoxins, causing acute kidney injury with muddy brown casts, impaired concentrating ability, and characteristic sodium wasting; recovery follows regeneration of the epithelium.

A reversible reduction in glomerular filtration caused by decreased effective circulating volume or renal perfusion, with avid tubular sodium and urea reabsorption; it resolves with restoration of perfusion and does not by itself cause tubular injury.

The percentage of filtered sodium excreted in urine, calculated from serum and urine sodium and creatinine; low values suggest prerenal states or glomerulonephritis, while high values suggest tubular injury, though diuretics confound interpretation.

A granular pigmented cast formed from degenerating tubular epithelial cells, seen in urine sediment in acute tubular necrosis and helpful in distinguishing intrinsic kidney injury from prerenal causes.

Functional kidney failure in advanced liver disease caused by splanchnic vasodilation and intense renal vasoconstriction, with minimal proteinuria and little structural damage; treatment includes vasoconstrictors and albumin.

A spectrum of disorders in which acute or chronic cardiac dysfunction and kidney dysfunction interact, largely through hemodynamic and neurohormonal mechanisms, producing congestion, reduced renal perfusion, and diuretic resistance.

Acute kidney injury occurring shortly after intravascular iodinated contrast administration, presumably from medullary ischemia and oxidative injury; risk is highest with preexisting kidney disease, diabetes, and volume depletion.

Metabolic emergency after rapid destruction of malignant cells, producing hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia; uric acid and calcium phosphate crystals can obstruct tubules and cause acute kidney injury.

Acute or chronic kidney injury from uric acid crystal deposition in tubules and interstitium, occurring with massive purine release or chronic hyperuricemia; prevention relies on hydration and urate-lowering therapy.

A calculated approximation of glomerular filtration rate from serum creatinine or cystatin C with age, sex, and race-free coefficients; it is used to stage chronic kidney disease and guide drug dosing and referral.

Excretion of albumin in urine, quantified by the albumin-to-creatinine ratio; persistent elevation indicates kidney damage, predicts progression and cardiovascular risk, and is graded to stage chronic kidney disease.

Classification of chronic kidney disease by glomerular filtration rate category (G1 to G5) combined with albuminuria category (A1 to A3), which together stratify risk of progression, cardiovascular events, and need for kidney replacement therapy.

An oral drug that blocks proximal tubular glucose and sodium reabsorption, lowering glucose and restoring tubuloglomerular feedback; it slows chronic kidney disease progression and reduces heart failure and kidney failure risk.

A local control mechanism in which the macula densa senses distal tubular sodium chloride delivery and adjusts afferent arteriolar tone, regulating single-nephron glomerular filtration rate and renin release.

Therapeutic inhibition of angiotensin II production or action with angiotensin-converting enzyme inhibitors or receptor blockers, lowering intraglomerular pressure and proteinuria and slowing chronic kidney disease progression.

Failure to achieve adequate natriuresis and fluid removal despite escalating loop diuretic doses, caused by distal sodium reabsorption, reduced tubular secretion, or post-diuretic sodium retention; management includes combination diuretics and dietary sodium restriction.

A drug inhibiting the sodium-potassium-2-chloride cotransporter in the thick ascending limb, producing the most powerful natriuresis; it also reduces medullary concentrating ability and can cause hypokalemia, hypocalcemia, and ototoxicity.

Serum potassium above the normal range, impairing cardiac conduction and neuromuscular function; causes include reduced kidney excretion, drugs blocking the renin-angiotensin-aldosterone axis, acidosis, and cell lysis, with treatment depending on severity and electrocardiographic changes.

A primary reduction in serum bicarbonate with compensatory hyperventilation, classified by the anion gap and by urinary measures of acid excretion; it can cause bone demineralization, muscle wasting, and accelerated kidney disease progression.

The difference between measured serum cations and anions, used to detect unmeasured acids such as ketones, lactate, or toxins; correction for albumin and calculation of the delta gap help classify metabolic acidosis.

Serum sodium concentration below normal, reflecting a disturbance in water balance relative to solute; classification by tonicity and volume status guides treatment, with overly rapid correction risking osmotic demyelination.

Neurologic injury from overly rapid correction of chronic hyponatremia, causing pontine and extrapontine demyelination with dysarthria, quadriparesis, and altered consciousness; prevention requires limiting the rate of sodium rise.

Euvolemic hypotonic hyponatremia caused by inappropriately concentrated urine from excess antidiuretic hormone or enhanced renal sensitivity, diagnosed after excluding hypothyroidism, adrenal insufficiency, and diuretic use.

A measure of delivered dialysis dose, commonly the urea clearance-time product normalized to urea distribution volume (Kt/V), used to ensure sufficient small-solute removal and to predict outcomes in maintenance dialysis patients.

A surgically created connection between an artery and vein, usually in the forearm, that enlarges and arterializes the vein to provide durable vascular access for hemodialysis with lower infection risk than catheters.

A home-based kidney replacement therapy in which dialysate instilled into the peritoneal cavity removes solutes by diffusion and fluid by osmotic ultrafiltration across the peritoneal membrane.

Immune attack by donor T lymphocytes against recipient tissues after allogeneic transplantation, causing rash, diarrhea, and liver injury; it is distinct from rejection, in which the host attacks the graft.

Host T-cell-mediated immune injury to a transplanted kidney, often presenting with rising creatinine and interstitial lymphocytic infiltrate with tubulitis; it is treated with corticosteroids and intensified immunosuppression.

An immunosuppressant such as tacrolimus or cyclosporine that blocks T-cell activation, preventing transplant rejection but causing dose-dependent afferent arteriolar vasoconstriction, hypertension, hyperkalemia, and chronic nephrotoxicity.

Formation of crystalline stones within the urinary tract, most commonly calcium oxalate or calcium phosphate, presenting with colicky flank pain and hematuria; composition and metabolic risk factors guide prevention.

Excessive urinary calcium excretion, a common risk factor for calcium stone formation; it may be absorptive, resorptive from bone, or renal in origin and is managed with hydration and dietary or pharmacologic measures.

An inherited disorder caused by mutations in PKD1 or PKD2, producing progressive bilateral renal cysts, hypertension, kidney enlargement, and eventual kidney failure, often with hepatic cysts and intracranial aneurysms.

A selective vasopressin V2 receptor antagonist that increases free water excretion; it slows cyst growth and kidney function decline in autosomal dominant polycystic kidney disease but can cause liver injury and requires monitoring.

Hereditary type IV collagen defect causing hematuria, progressive kidney failure, sensorineural hearing loss, and ocular abnormalities; inheritance is often X-linked, and angiotensin blockade slows progression.

Drug- or infection-triggered inflammation of the tubulointerstitium, presenting with acute kidney injury, sterile pyuria, white cell casts, and sometimes fever, rash, or eosinophilia; withdrawal of the culprit drug is central to management.

A urinary cast containing leukocytes, indicating inflammation within renal tubules or interstitium; it suggests acute interstitial nephritis or pyelonephritis rather than glomerular or prerenal disease.

Kidney injury linked to proton pump inhibitor use, most often acute interstitial nephritis but also chronic interstitial fibrosis and hypomagnesemia; it should be considered in unexplained acute kidney injury with sterile pyuria.

Narrowing of a main or branch renal artery, usually from atherosclerosis or fibromuscular dysplasia, causing hypertension and sometimes ischemic nephropathy; angiotensin blockade requires caution because it can precipitate acute kidney injury.

Severe blood pressure elevation with acute target-organ injury such as encephalopathy, retinal hemorrhage, or kidney injury; it requires controlled parenteral blood pressure reduction to avoid ischemic complications.

Microvascular injury with platelet-rich thrombi causing hemolytic anemia, thrombocytopenia, and organ ischemia, including kidney failure; causes include complement dysregulation, drugs, and hypertension, and treatment targets the underlying mechanism.

An abrupt decline in kidney function over hours to days, defined by a rise in serum creatinine or fall in urine output; it is staged by severity and classified as prerenal, intrinsic, or postrenal.

Perioperative acute kidney injury after cardiac surgery caused by hemodynamic instability, inflammation, hemolysis, and emboli; it is associated with increased mortality and often requires careful fluid and vasopressor management.

Sustained intra-abdominal pressure elevation that impairs venous return and renal perfusion, causing oliguric acute kidney injury; decompression is the definitive treatment and is often required in critically ill patients.