CNN-NP key terms

The volume of plasma filtered by the glomeruli per unit time, usually expressed in mL/min. Estimated GFR from serum creatinine plus age, sex, and race-free equations is used to stage chronic kidney disease.

Classification of CKD by GFR category (G1 to G5) and albuminuria category (A1 to A3). Both dimensions predict progression and cardiovascular risk, so staging always reports the pair.

A spot urine measurement that estimates 24-hour albumin excretion by dividing albumin by creatinine, correcting for urine concentration. Values of 30 mg/g or higher define albuminuria and are a key CKD prognostic marker.

The volume of plasma cleared of creatinine per minute, reflecting glomerular filtration. Measured by timed urine collection or estimated by Cockcroft-Gault, which remains common for drug dose adjustment.

An abrupt decline in kidney function defined by a creatinine rise of at least 0.3 mg/dL within 48 hours, a rise to 1.5 times baseline within 7 days, or urine output below 0.5 mL/kg/h for 6 hours.

A reversible rise in creatinine caused by reduced renal perfusion, such as volume depletion or heart failure, without intrinsic tubular damage. It typically improves rapidly with restoration of perfusion.

Intrinsic kidney injury from ischemic or nephrotoxic insult causing tubular cell damage. It produces muddy brown granular casts, impaired concentrating ability, and often a prolonged recovery phase.

The percentage of filtered sodium excreted in urine, calculated from paired serum and urine sodium and creatinine. Values below 1 percent suggest prerenal physiology; higher values suggest intrinsic injury, though diuretics confound results.

The percentage of filtered urea excreted in urine, used when diuretics make fractional excretion of sodium unreliable. Values below 35 percent suggest a prerenal state.

Pigmented granular casts seen on urine microscopy in acute tubular necrosis, formed from degenerated tubular cells. Their presence supports intrinsic renal injury over a prerenal cause.

Examination of spun urine sediment for cells, casts, crystals, and organisms. Findings such as red cell casts, dysmorphic red cells, or fatty casts narrow the differential diagnosis of kidney disease.

Cylindrical structures formed when red cells are trapped in tubular lumen protein and molded there. They indicate glomerular bleeding and are a hallmark of glomerulonephritis.

A clinical complex of heavy proteinuria above 3.5 g per day, hypoalbuminemia, edema, and hyperlipidemia. It reflects glomerular podocyte injury and carries high thrombotic and infection risk.

Urine protein excretion exceeding 3.5 g per day, or a spot protein-to-creatinine ratio above roughly 3500 mg/g. It defines the proteinuria threshold of nephrotic syndrome.

A podocyte disorder causing nephrotic syndrome with normal glomeruli on light microscopy and foot process effacement on electron microscopy. It is the most common nephrotic cause in children and responds well to corticosteroids.

A glomerular lesion with sclerosis of some glomeruli and portions of each affected tuft, often causing nephrotic syndrome. It is associated with HIV, obesity, vesicoureteral reflux, and APOL1 risk variants.

A glomerular disease with subepithelial immune deposits causing nephrotic syndrome in adults. Anti-phospholipase A2 receptor antibodies are a key serologic marker and guide monitoring.

An autoantibody directed at the phospholipase A2 receptor on podocytes, found in most primary membranous nephropathy cases. Titers correlate with disease activity and can guide treatment decisions.

The most common primary glomerulonephritis worldwide, caused by IgA-containing immune deposits in the mesangium. It often presents with gross hematuria after an upper respiratory infection.

Inflammation of the glomeruli from immune-mediated injury, producing hematuria, proteinuria, hypertension, and reduced filtration. It may be primary or secondary to systemic disease such as lupus.

An autoimmune disorder in which antibodies attack type IV collagen in the glomerular and alveolar basement membranes. Lung and kidney involvement together is called Goodpasture syndrome.

An inherited disorder in which numerous cysts enlarge the kidneys and progressively destroy parenchyma. Autosomal dominant disease also causes liver cysts and intracranial aneurysms.

A selective vasopressin V2 receptor antagonist that slows cyst growth and GFR decline in autosomal dominant polycystic kidney disease. It causes aquaresis and requires monitoring of liver enzymes and sodium.

Structured counseling that presents hemodialysis, peritoneal dialysis, and kidney transplantation with their lifestyle and outcome implications. It should begin well before dialysis is needed so patients can choose with adequate time.

Confirmation that a dialysis prescription delivers sufficient clearance and volume control, commonly measured by Kt/V urea and ultrafiltration achievement. Inadequate clearance raises morbidity and mortality risk.

A dimensionless measure of dialysis clearance in which K is urea clearance, t is treatment time, and V is urea distribution volume. Higher values indicate more delivered dialysis dose.

A surgically created connection between an artery and a vein, usually in the forearm, that enlarges the vein for repeated dialysis access. It is the preferred access because it lasts longer and infects less than catheters.

A systemic infection attributed to a central venous dialysis catheter, diagnosed by positive blood cultures with no other source. It requires prompt antimicrobial therapy and often catheter removal.

A home dialysis modality in which dialysate is instilled into the peritoneal cavity and solute exchange occurs across the peritoneal membrane. It preserves residual kidney function and offers flexible scheduling.

Infection of the peritoneal cavity in a peritoneal dialysis patient, marked by cloudy effluent, abdominal pain, and elevated effluent white cell count. Intraperitoneal antibiotics are started after effluent culture.

The process of evaluating and registering a candidate for a deceased-donor kidney, including immunologic and medical assessment. Early referral improves access and allows preemptive transplantation.

An immunosuppressant class including tacrolimus and cyclosporine that blocks T-cell activation. These drugs prevent transplant rejection but cause nephrotoxicity, hypertension, and drug interactions via cytochrome P450.

The blood concentration of tacrolimus measured just before the next dose, used to titrate immunosuppression after transplant. Targets vary with time since transplant and rejection risk.

Treatment of elevated serum potassium using cardiac membrane stabilization with calcium, intracellular shift with insulin and beta agonists, and potassium removal through diuretics, binders, or dialysis.

An oral nonabsorbed polymer that exchanges sodium and hydrogen for potassium in the gut, lowering serum potassium. It is used chronically in CKD and heart failure to permit renin-angiotensin system inhibitor therapy.

A normal anion gap acidosis from reduced renal acid excretion and bicarbonate generation. Treatment with oral bicarbonate may slow progression and improve nutritional status.

A drug class including ACE inhibitors and angiotensin receptor blockers that reduces intraglomerular pressure and albuminuria. It slows CKD progression but requires monitoring of potassium and creatinine.

A drug that blocks sodium-glucose cotransport in the proximal tubule, lowering glucose and intraglomerular pressure. In CKD it slows GFR decline and reduces heart failure hospitalization independent of diabetes status.

An agent such as furosemide that blocks the sodium-potassium-chloride cotransporter in the thick ascending limb, producing strong natriuresis. It is used for volume overload in CKD and nephrotic syndrome.

Failure to achieve adequate natriuresis despite escalating loop diuretic doses, often from distal sodium reabsorption, reduced tubular delivery, or dietary sodium excess. Management includes combination diuretic therapy and sodium restriction.

A serum sodium below the normal range, classified by volume status and tonicity. Correction rate matters because overly rapid correction can cause osmotic demyelination.

Neurologic injury from overly rapid correction of chronic hyponatremia, causing pontine and extrapontine myelin damage. It presents with dysarthria, dysphagia, confusion, or quadriparesis days after correction.

Adjustment of medication dose or interval based on estimated kidney function and drug clearance pathways. It prevents accumulation toxicity for renally eliminated drugs and their active metabolites.

Clinical practice of identifying and limiting exposure to drugs and agents that injure the kidney, such as aminoglycosides, iodinated contrast, and NSAIDs. It includes dose limits and hydration when exposure is unavoidable.

An acute rise in creatinine after intravascular iodinated contrast administration, occurring when no other cause is identified. Risk is highest with preexisting kidney disease, diabetes, and volume depletion.

Functional kidney failure in advanced liver disease from splanchnic vasodilation and renal vasoconstriction, without structural kidney damage. It is treated with vasoconstrictors plus albumin and is reversed by liver transplantation.

Extracorporeal removal of plasma and its pathogenic antibodies or proteins, followed by replacement fluid. It is used in anti-glomerular basement membrane disease and some antibody-mediated transplant rejection.