Kidney Anatomy, Physiology, and Clinical Nephrology

Vocabulary practice flashcards covering renal anatomy, countercurrent physiology, electrolyte and acid-base disorders, biomarkers, and clinical nephrology.

Total Body Water (TBW)

The total volume of fluid in the body, accounting for approximately $60\%$ of body weight in adult men ($36\,\text{L}$ in a $60\,\text{kg}$ man) and $50\%$ in adult women, partitioned into intracellular fluid ($\approx 2/3$, $24\,\text{L}$) and extracellular fluid ($\approx 1/3$, $12\,\text{L}$).

Effective Arterial Blood Volume (EABV)

The proportion of circulating blood volume within the arterial tree ($\approx 15\%$ of plasma) that perfuses tissues and stimulates baroreceptors; a urinary sodium concentration $<20\,\text{mEq/L}$ typically indicates reduced EABV in the setting of preserved tubular function.

Glomerular Filtration Barrier

A trilaminar selectively permeable filter comprising fenestrated capillary endothelium, a glomerular basement membrane that restricts protein passage, and visceral epithelial podocyte foot processes bridged by slit diaphragms containing nephrin and podocin.

Juxtaglomerular Apparatus (JGA)

A specialized regulatory microvascular structure located where the distal tubule contacts its parent glomerulus, composed of macula densa cells, afferent and efferent arteriolar smooth muscle cells, and granular Goormaghtigh cells that secrete renin.

Tubuloglomerular Feedback

An intrinsic renal autoregulatory mechanism where elevated $\text{Na}^+\text{Cl}^-$ delivery sensed by the macula densa triggers afferent arteriolar vasoconstriction to lower GFR, whereas reduced $\text{Na}^+\text{Cl}^-$ delivery stimulates renin release and efferent arteriolar constriction.

$$\text{Na}^+/\text{H}^+\text{-Exchanger 3 (NHE3)}$$

An apical sodium-hydrogen antiporter in proximal convoluted tubular epithelial cells responsible for reabsorbing the majority of filtered sodium and facilitating the reclamation of filtered bicarbonate into the bloodstream.

$$\text{Na}^+/\text{K}^+/2\text{Cl}^-\text{ Cotransporter (NKCC2)}$$

An apical symporter in the thick ascending limb of the loop of Henle responsible for reabsorbing $25\%$ of filtered sodium; it is inhibited by loop diuretics (e.g., furosemide) and genetically impaired in Bartter syndrome.

$$\text{Na}^+/\text{Cl}^-\text{ Cotransporter (NCC)}$$

An apical sodium-chloride cotransporter localized to the distal convoluted tubule that reabsorbs approximately $5\%$ of filtered sodium; it is inhibited by thiazide diuretics (e.g., chlorthalidone) and genetically defective in Gitelman syndrome.

Epithelial Sodium Channel (ENaC)

A luminal membrane channel in cortical collecting duct principal cells that mediates sodium reabsorption under positive regulation by aldosterone; it is directly inhibited by potassium-sparing diuretics (e.g., amiloride) and indirectly downregulated by mineralocorticoid receptor antagonists (e.g., spironolactone).

Glomerular Filtration Rate (GFR)

The total volume of fluid filtered from the glomerular capillaries into Bowman's space per unit time across all functioning nephrons in both kidneys, averaging $120\,\text{mL/min}$ in young women, $130\,\text{mL/min}$ in young men, and normalized to a body surface area of $1.73\,\text{m}^2$.

Renal Clearance ($Cl$)

The virtual volume of arterial plasma completely cleared of a given substance by the kidneys per unit time, expressed by the formula $Cl = \frac{V \times U}{P}$, where $V$ is urine flow rate ($\text{mL/min}$), $U$ is urine solute concentration, and $P$ is plasma solute concentration.

Cystatin C

A low-molecular-weight endogenous protein produced at a constant rate by all nucleated cells, freely filtered at the glomerulus, and $99\%$ reabsorbed and catabolized by proximal tubular cells; measured in plasma as a filtration marker unaffected by muscle mass, age, or sex.

Isosthenuria

The excretion of urine with a fixed specific gravity of $1.010$, matching that of protein-free plasma filtrate, indicating complete loss of renal medullary tubular concentrating and diluting abilities.

Pseudohyponatremia

An in vitro measurement artifact where marked elevation of circulating solids—such as severe hypertriglyceridemia ($>1500\,\text{mg/dL}$) or hyperproteinemia ($>10\,\text{g/dL}$)—displaces plasma water volume, producing an artificially low total plasma sodium measurement despite normal physiological aqueous sodium concentration and osmolality.

Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

A clinical condition of euvolemic hypotonic hyponatremia driven by non-physiologic release of arginine vasopressin (AVP), marked by concentrated urine (osmolality $>100\,\text{mOsm/kg}$) and high urinary sodium ($\ge 30\,\text{mmol/L}$) in the absence of renal, cardiac, adrenal, or thyroid disease.

Central Diabetes Insipidus

A disorder caused by deficient hypothalamic synthesis or posterior pituitary release of antidiuretic hormone (ADH), presenting with severe polyuria ($>2\,\text{L/day}$), polydipsia, low urine osmolality, and a prompt corrective response to exogenous desmopressin.

Nephrogenic Diabetes Insipidus

A defect in renal concentrating ability caused by collecting duct unresponsiveness to circulating antidiuretic hormone, characterized by polyuria, polydipsia, failure to concentrate urine above $300\text{--}600\,\text{mOsm/kg}$, and no response to exogenous vasopressin.

Bartter Syndrome

An autosomal recessive tubulopathy affecting the thick ascending limb of Henle (most commonly NKCC2 or ROMK mutations) characterized by childhood presentation, severe renal salt wasting, hypokalemic metabolic alkalosis, hypercalciuria, nephrocalcinosis, and hyperreninemic hyperaldosteronism with normal blood pressure.

Gitelman Syndrome

An autosomal recessive tubulopathy involving loss-of-function mutations in the distal convoluted tubule $\text{Na}^+/\text{Cl}^-$ cotransporter (NCC), typically presenting in adulthood with mild salt wasting, hypokalemic metabolic alkalosis, hypocalciuria, hypomagnesemia, and a blunted fractional excretion of chloride during a hydrochlorothiazide challenge ($<2.3\%$).

Autosomal Dominant Polycystic Kidney Disease (ADPKD)

A genetic condition caused by mutations in PKD1 ($85\%$) or PKD2, leading to diminished intracellular calcium, elevated intracellular $\text{cAMP}$, protein kinase A activation, aberrant tubular cell proliferation, and progressive fluid-filled cyst expansion that causes kidney failure.

Tolvaptan

A selective vasopressin V2-receptor antagonist that reduces intracellular $\text{cAMP}$ generation within distal nephron and collecting duct epithelial cells, slowing renal cyst cell proliferation and fluid secretion in patients with ADPKD.

Horseshoe Kidney

A congenital renal fusion anomaly wherein the lower poles of both kidneys fuse across the midline anterior to the great vessels before ascent, frequently resulting in urinary stasis, hydronephrosis, and calcium oxalate calculi formation.

Acute Kidney Injury (KDIGO Criteria)

An abrupt decline in kidney filtration defined by an increase in serum creatinine by $\ge 0.3\,\text{mg/dL}$ ($\ge 26.5\,\mu\text{mol/L}$) within 48 hours, an increase in serum creatinine to $\ge 1.5\times$ baseline within 7 days, or a reduction in urine volume to $<0.5\,\text{mL/(kg}\cdot\text{h)}$ for at least 6 hours.

Hepatorenal Syndrome (HRS)

A functional, reversible acute kidney injury occurring in patients with advanced cirrhosis or fulminant hepatic failure, characterized by marked splanchnic arterial vasodilation and intense compensatory renal vasoconstriction, resulting in severe reductions in GFR and renal blood flow.

Calcium Gluconate (in Hyperkalemia)

An intravenous membrane-stabilizing therapy administered to antagonize potassium-induced cardiac toxicity and prevent life-threatening ventricular arrhythmias within 1 to 3 minutes; it acts without altering serum potassium concentrations.

Sodium Zirconium Cyclosilicate

An insoluble, non-absorbed, highly selective inorganic crystalline cation exchanger that traps potassium in the gastrointestinal tract in exchange for sodium and hydrogen ions, utilized to treat hyperkalemia in chronic kidney disease and heart failure.

Patiromer

A non-absorbed organic polymer that binds potassium in exchange for calcium within the gastrointestinal tract, promoting fecal potassium elimination and lowering serum potassium without increasing dietary sodium absorption.

Fibroblast Growth Factor 23 (FGF-23)

A bone-derived phosphaturic hormone that decreases proximal tubular phosphate reabsorption and suppresses renal $1\alpha\text{-hydroxylase}$, thereby reducing active $1,25\text{-dihydroxyvitamin D}$ synthesis and downregulating parathyroid hormone production.

Calcitriol ($1,25\text{-Dihydroxyvitamin D}$)

The biologically active hormonal metabolite of vitamin D synthesized by renal proximal tubular cells, responsible for enhancing intestinal calcium and phosphate absorption, stimulating bone remodeling, and exerting negative feedback on parathyroid hormone secretion.

Serum Anion Gap (AG)

The difference between routinely measured serum cations and anions, calculated as $\text{AG} = [\text{Na}^+] - ([\text{Cl}^-] + [\text{HCO}_3^-])$, with a normal range of $8\text{--}12\,\text{mEq/L}$, reflecting unmeasured serum anions including albumin, phosphate, sulfate, and organic acids.

Type 1 Distal Renal Tubular Acidosis

A tubular acid-base disturbance characterized by impaired collecting duct hydrogen ion ($\text{H}^+$) secretion, resulting in an inability to lower urine pH below $5.5$ in the presence of systemic acidemia, accompanied by a positive urine anion gap, hypokalemia, hypocitraturia, and nephrocalcinosis.

Type 2 Proximal Renal Tubular Acidosis

A disorder of proximal tubular bicarbonate reclamation resulting in a lowered renal absorptive threshold (from $24\,\text{mmol/L}$ down to $\approx 15\,\text{mmol/L}$), leading to transient bicarbonaturia, normal anion gap metabolic acidosis, and hypokalemia until plasma bicarbonate stabilizes at the lower setpoint.

Type 4 Renal Tubular Acidosis

A distal tubule disorder resulting from aldosterone deficiency or resistance (hyporeninemic hypoaldosteronism), characterized by impaired renal excretion of both hydrogen and potassium ions, presenting as a normal anion gap hyperchloremic metabolic acidosis with hyperkalemia.

Saline-Responsive Metabolic Alkalosis

A state of elevated plasma bicarbonate and metabolic alkalosis initiated and maintained by extracellular fluid volume contraction, potassium loss, and chloride depletion (urinary chloride $<10\text{--}20\,\text{mEq/L}$), which is corrected by the administration of isotonic ($0.9\%$) sodium chloride.