[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [Physiology](https://durgical.com/en/physiology/) › [Renal, fluids and acid–base](https://durgical.com/en/physiology/#s-renal) › Physiology of acute and chronic kidney failure [Physiology](https://durgical.com/en/physiology/) · [Renal, fluids and acid–base](https://durgical.com/en/physiology/#s-renal) # Physiology of acute and chronic kidney failure - Mechanism - Exam priority: medium When the kidneys filter too little, potassium, acid, water and wastes build up and kidney hormones fail; cause and speed shape the picture. Updated 2026-11-01 Also called: Renal failure, Uraemia, Hyperfiltration **See it in 3D:** [Kidneys](https://durgical.com/en/anatomy/kidney/) ## Key points - Prerenal: a healthy tubule saving sodium (FENa 20, concentrated urine). - Acute tubular necrosis: the damaged tubule cannot save sodium or concentrate (FENa > 2 %, muddy brown granular casts, near-isosmotic urine). - Postrenal: Bowman’s capsule pressure rises and GFR falls; only if both kidneys (or a single functioning one) are obstructed. - CKD: hyperfiltration in remaining nephrons; ACE inhibitors and ARBs lower intraglomerular pressure and protect. - Consequences of CKD: hyperkalaemia (late), metabolic acidosis, phosphate retention with high FGF-23 and PTH, low calcitriol, anaemia from low erythropoietin, hypertension. - Isosthenuria: in advanced CKD urine is fixed near 300 mOsm/kg (it neither concentrates nor dilutes). ## What it is Acute kidney injury (AKI) is a fall in filtration over hours to days; chronic kidney disease (CKD) is loss of function or damage lasting more than three months. In AKI, location matters: before the kidney (poor perfusion), in the kidney (tubular necrosis, glomerulonephritis, interstitial nephritis) or after it (obstruction). In CKD the surviving nephrons adapt by filtering more (hyperfiltration), which preserves function for a while but speeds their own damage. ## How it works, step by step - As nephrons are lost, the solute load is shared among fewer units: each one filters and excretes more. - Angiotensin II and afferent dilation raise glomerular pressure in those nephrons (hyperfiltration). - High pressure injures podocytes: proteinuria, glomerulosclerosis and loss of more nephrons (a vicious circle). - Retained phosphate stimulates FGF-23 and PTH, which at first keep phosphate normal at the expense of bone. - FGF-23 and loss of renal mass lower calcitriol: less calcium absorption and more PTH (secondary hyperparathyroidism). - Fewer nephrons make less ammonium: daily acid is not cleared and acidosis appears. - Potassium holds until late stages because each remaining nephron secretes more K⁺ (aldosterone, high flow). ### The nephron: segments, transporters and diuretics **GFR** ≈ 125 mL/min **Filtrate** ≈ 180 L/day **Urine** ≈ 1–2 L/day Tap a nephron segment: what it reabsorbs, its transporters, the hormones, the diuretics that act there and the classic disorders. - Glomerulus and arterioles - Proximal tubule - Thin descending limb - Thin ascending limb - Thick ascending limb - Distal convoluted tubule - Collecting tubule and duct - Juxtaglomerular apparatus (macula densa) - Cortex - Medulla - Interstitial osmolality (≈ 300 → 1200 mOsm/kg) Illustrative schematic drawn by Durgical (a long-loop juxtamedullary nephron); proportions and percentages are approximate and not for clinical decisions. ## Equations **Fractional excretion of sodium**FENa (%) = (UNa × PCr) / (PNa × UCr) × 100 Less useful with diuretics (which raise it) or with prior CKD. ## CKD stages by glomerular filtration rate (KDIGO) | Stage | GFR (mL/min/1.73 m²) | Description | | --- | --- | --- | | [G1](https://durgical.com/en/conditions/chronic-kidney-disease/) | ≥ 90 | Normal or high, with a marker of damage (albuminuria) | | G2 | 60–89 | Mildly decreased | | G3a | 45–59 | Mildly to moderately decreased | | G3b | 30–44 | Moderately to severely decreased | | G4 | 15–29 | Severely decreased | | G5 | - Diabetes and hypertension are the leading causes of CKD in Colombia and worldwide; albuminuria is the first sign and predicts progression. - NSAIDs in a patient with low volume or heart failure remove prostaglandin-driven afferent dilation and can precipitate AKI. - Creatinine lags after an acute injury: in the first hours it can be normal although GFR has already fallen. ## Memory aid “Prerenal saves, tubular spills, postrenal dams”: sodium kept, sodium lost, urine stuck. ## Test yourself Think of the answer, then tap the question to see it. ## Why is FENa low in prerenal AKI and high in acute tubular necrosis? In prerenal AKI the tubule is healthy and, with RAAS active, reabsorbs nearly all sodium. In tubular necrosis the damaged cells cannot reabsorb it, so a larger fraction is lost. ## How does CKD produce secondary hyperparathyroidism? Phosphate is retained and FGF-23 rises, which together with lost renal mass lowers calcitriol; calcium absorption and ionised calcium fall, and high phosphate directly stimulates the parathyroids: PTH rises. ## Why can ACE inhibitors raise creatinine a little when started and still protect the kidney long term? They dilate the efferent arteriole and lower glomerular pressure: GFR dips slightly, but the hyperfiltration and proteinuria that damage the remaining nephrons are reduced. ## Why is the anaemia of CKD normocytic and responsive to erythropoietin? The main problem is low renal erythropoietin production; the marrow is healthy and makes normal red cells in insufficient numbers. [Add to my cards (4)](https://durgical.app/estudiar/?add=/en/physiology/physiology-of-acute-and-chronic-kidney-failure/) ## See it in 3D The structures of Durgical's 3D anatomy where it happens. - [Kidneys](https://durgical.com/en/anatomy/kidney/) ## Related topics - [Measuring GFR and plasma flow: inulin, creatinine, PAH and filtration fraction](https://durgical.com/en/physiology/measuring-gfr-and-plasma-flow-inulin-creatinine-pah-and-filtration-fraction/) - [Glomerular filtration: the barrier and its determinants](https://durgical.com/en/physiology/glomerular-filtration-the-barrier-and-its-determinants/) - [Renal clearance](https://durgical.com/en/physiology/renal-clearance/) - [Potassium balance](https://durgical.com/en/physiology/potassium-balance/) - [Renal handling of H⁺ and bicarbonate](https://durgical.com/en/physiology/renal-handling-of-h-and-bicarbonate/) - [Phosphate and FGF-23](https://durgical.com/en/physiology/phosphate-and-fgf-23/) - [Erythropoiesis and erythropoietin](https://durgical.com/en/physiology/erythropoiesis-and-erythropoietin/) ## Related conditions - [Acute kidney injury](https://durgical.com/en/conditions/acute-kidney-injury/) - [Chronic kidney disease](https://durgical.com/en/conditions/chronic-kidney-disease/) - [Hyperkalaemia](https://durgical.com/en/conditions/hyperkalaemia/) - [Hypocalcaemia](https://durgical.com/en/conditions/hypocalcaemia/) - [Arterial hypertension](https://durgical.com/en/conditions/arterial-hypertension/) ## In Biochemistry - [Creatinine and estimated glomerular filtration rate (eGFR)](https://durgical.com/en/biochemistry/topics/creatinine-and-estimated-glomerular-filtration-rate/) - [Urea and blood urea nitrogen (BUN) as lab tests](https://durgical.com/en/biochemistry/topics/urea-and-blood-urea-nitrogen-as-lab-tests/) - [Urinalysis](https://durgical.com/en/biochemistry/topics/urinalysis/) ## In Pharmacology - [ACE inhibitors](https://durgical.com/en/pharmacology/classes/ace-inhibitors/) - [Nonsteroidal anti-inflammatory drugs (NSAIDs)](https://durgical.com/en/pharmacology/classes/nonsteroidal-anti-inflammatory-drugs/) [← All of physiology](https://durgical.com/en/physiology/) Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given. Sources: [Acute Kidney Injury](https://www.ncbi.nlm.nih.gov/books/NBK441896/) (StatPearls (NCBI Bookshelf), 2024); [Chronic Kidney Disease](https://www.ncbi.nlm.nih.gov/books/NBK535404/) (StatPearls (NCBI Bookshelf), 2024); [25.5 Physiology of Urine Formation](https://openstax.org/books/anatomy-and-physiology-2e/pages/25-5-physiology-of-urine-formation) (OpenStax (Rice University), 2022); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 32). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016). ## **Spotted a mistake?** We are always improving for the community. Tell us what is wrong and our team will review it. Report a mistake Representative model, for educational purposes only. --- Source: https://durgical.com/en/physiology/physiology-of-acute-and-chronic-kidney-failure/ License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/physiology/physiology-of-acute-and-chronic-kidney-failure/