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Each kidney contains ~1 million nephrons, the functional units of filtration. The nephron consists of a glomerulus (filtration of blood plasma into Bowman's capsule), proximal convoluted tubule (bulk reabsorption of glucose, amino acids, Na⁺, water), loop of Henle (countercurrent multiplication creating the medullary concentration gradient), distal convoluted tubule (fine-tuning of ion balance), and collecting duct (water reabsorption under ADH). Filtration is driven by hydrostatic pressure in the glomerular capillaries; ~180 L of filtrate forms per day but only ~1.5 L is excreted as urine. The renin-angiotensin-aldosterone system (RAAS) and antidiuretic hormone (ADH) regulate blood pressure and osmolarity through the kidney.
Trace a filtrate molecule through each nephron segment, noting what is added or removed at each step. Work through acid-base disorders (respiratory vs. metabolic acidosis/alkalosis) to understand renal compensation.
From your study of homeostasis and renal physiology, you know the kidney regulates fluid balance and blood pressure. Understanding how requires tracing the path of fluid through the nephron — the kidney's functional unit — and seeing how each segment contributes to the kidney's broader regulatory role.
Filtration begins at the glomerulus, a tuft of high-pressure capillaries enclosed by Bowman's capsule. Hydrostatic pressure forces water, ions, glucose, amino acids, urea, and other small molecules through the fenestrated capillary walls into the capsule, forming the filtrate. Proteins and blood cells are too large to pass and remain in the blood. This is a bulk, non-selective process: the kidney doesn't choose what to filter — it filters almost everything small, then selectively reclaims what the body needs. About 180 liters of filtrate forms per day, which sounds alarming until you realize that roughly 99% is reabsorbed.
The proximal convoluted tubule (PCT) performs the heaviest lifting. Active transporters in PCT cells recover virtually all filtered glucose and amino acids, and osmosis follows the sodium being pumped out, drawing water with it. This explains why glucosuria is abnormal: the PCT has sufficient transport capacity to reclaim all filtered glucose at normal blood sugar levels. Only when glucose exceeds ~180 mg/dL — saturating the transporters — does any spill into urine, which is why glucosuria is a clinical indicator of poorly controlled diabetes.
The loop of Henle creates the kidney's essential tool for concentrating urine. As filtrate descends into the medulla, it loses water by osmosis into an increasingly salty interstitium. The ascending limb then pumps sodium chloride out without allowing water to follow, building a steep osmotic gradient in the medullary tissue. The collecting duct passes through this gradient on its way back out; under antidiuretic hormone (ADH), aquaporin channels open in the collecting duct wall and water is drawn out by osmosis, producing concentrated urine. Without ADH — as in diabetes insipidus — the collecting duct remains impermeable and large volumes of dilute urine are produced.
Finally, the kidney is deeply integrated with blood pressure regulation through the renin-angiotensin-aldosterone system (RAAS). When blood pressure falls, juxtaglomerular cells in the afferent arteriole release renin, triggering a cascade that produces angiotensin II, which raises blood pressure directly (vasoconstriction) and indirectly (stimulating aldosterone to increase sodium reabsorption in the distal tubule, expanding blood volume). This feedback loop is why ACE inhibitors — which block a key step in the RAAS cascade — are effective antihypertensives, and why renal disease so often causes hypertension.