Each fist-sized kidney holds a million nephrons: glomerulus for filtering, then a tubule that edits the filtrate segment by segment — proximal bulk reabsorption, loop countercurrent concentration, distal fine-tuning, collecting duct hormonal control. The kidney is also a metabolic organ: it gluconeogenizes in fasting (a rival to liver), activates vitamin D, and runs its outer medulla at the edge of hypoxia to preserve the osmotic gradient.
Metabolic Pathways
Filtration-reabsorption: 180 liters filtered, over 99 percent reclaimed — the tubule's energy bill explains the organ's oxygen hunger.
Fasting gluconeogenesis from lactate and glutamine — see the glutamine pathways.
Ammoniagenesis from glutamine buffers acid load, excreted as ammonium.
Regulation
RAAS: renin release couples filtration, pressure, and aldosterone-driven sodium retention.
Vasopressin sets collecting-duct water permeability — urine concentration on demand.
Tubuloglomerular feedback steadies each nephron's own flow rate.
Interactions
Erythropoietin output links it to hemoglobin and oxygen sensing.
With the liver, it co-manages acid-base — the urea cycle's product is its nitrogen cargo.
Downstream plumbing is the urinary system; the excretory overview is here.
Clinical Relevance
Chronic kidney disease: nephrons lost silently over decades — diabetes and hypertension the main drivers.
Acute kidney injury is the ICU's metabolic emergency; dialysis substitutes for filtration.
Polycystic disease and glomerulonephritis are the classic structural and immunologic diseases.
The kidney cannot make new nephrons after birth — every one lost is lost for good.
Estimated GFR from creatinine is the clinic's proxy for the organ's filtration capacity.
Endocrine Functions
Content consolidated from the former Kidney (Endocrine) page.
The heart's natriuretic peptides act on the kidney — see the endocrine heart.
FGF23 from bone suppresses its calcitriol — an endocrine feedback between organs.
Its renin axis is the pharmacology of ACE inhibitors, ARBs, and renin inhibitors.
Renal anemia is EPO deficiency treated with recombinant hormone — dialysis patients its first beneficiaries.
Renovascular hypertension is the renin axis gone structural.
Secondary hyperparathyroidism of kidney disease is the mineral axis failing as a unit — EPO, renin, and vitamin D axes fail in the same patient, one organ's disease.
Recombinant EPO changed dialysis medicine — and its athletic abuse wrote a chapter of sports pharmacology.