--- module: 020-02 language: en chapter: 20 title: "Acute Kidney Injury, Chronic Kidney Disease, and Renal Pharmacology" module_title: "Kidney injury phenotypes, recovery trajectories, and replacement decisions" source_sha256: 730abd69efc1ba2f4e35d336761b4cac2ac3298e57aa5a4f6f210bd448031b09 --- # Kidney injury phenotypes, recovery, and replacement decisions ## Injury as a syndrome ### Loss of filtration or urine, not one lesion ### Haemodynamic, tubular, interstitial, glomerular, vascular, obstructive ### Pre-renal label suggests intact responsive tissue #### Prolonged stress becomes structural injury #### Tubular injury keeps reversible haemodynamic components ### Assess perfusion, congestion, exposure, sediment, trajectory ### Oliguria is earlier evidence but confounded ## Haemodynamic and congestive phenotypes ### Reduced filling activates sympathetic and hormonal responses #### Restoring pressure can reverse it before injury ### Congestion lowers the filtration gradient #### Impaired lymphatic drainage and sodium retention #### Repeated fluid for a rising creatinine worsens it ### Abdominal and airway pressure alter renal venous return ## Tubular injury and repair ### Lost polarity, redistributed transporters, obstructed lumens ### Back-leak, inflammation, vasoconstriction sustain low filtration ### Surviving cells dedifferentiate, migrate, proliferate #### Polyuric phase precedes restored concentrating capacity ### Maladaptive repair causes capillary loss and fibrosis #### Biochemical recovery can hide reduced reserve ### Pigment injury: toxicity, obstruction, vasoconstriction #### Potassium and calcium hazards precede creatinine ## Interstitial, glomerular, and vascular urgency ### Interstitial nephritis often lacks the classic triad ### Active sediment raises glomerular urgency #### Delay converts inflammation into crescents and scar ### Thrombotic microangiopathy: endothelium, platelets, haemolysis #### Selected mechanisms need time-critical specific treatment ### Vascular disease can give a bland urine ## Obstruction and decompression ### Continuing urine does not exclude obstruction ### Early blockage shows little hydronephrosis ### Chronic dilation persists without active pressure ### Decompression causes haematuria and diuresis #### Replace a proportion, not every millilitre ## Chronic progression and risk ### Filtration category and albuminuria are two dimensions #### Albumin predicts cardiovascular events #### Rate of change is the third dimension ### Hyperfiltration raises single-nephron pressure #### Filtered protein activates inflammation and fibrosis ### Blockade and cotransporter inhibition lower glomerular load #### Early filtration dip, better long-term trajectory ### Atypical patterns should not end investigation ## Dialysis and the decision to start ### Diffusion for solute, transmembrane pressure for water ### Clearance rises with flows, membrane, and time ### Rapid urea fall can swell the brain ### Continuous therapy trades speed for steady control #### Clotting and interruption reduce delivered dose ### Peritoneal dialysis uses capillaries and glucose gradient #### Cloudy effluent needs urgent sampling ### Start on refractory physiology, not creatinine #### Potassium, acidity, volume, uraemic effects, toxin #### Modality fits stability, urgency, access, plan ## Planning before replacement ### Preparation does not begin just before dialysis ### Share progression rate and replacement possibility ### Transplantation, home therapy, in-centre dialysis, conservative care ### Explained against values and daily life ### Access, vaccination, anaemia and bone-mineral care ### Nutrition, medication education, symptom relief ### Frailty: travel burden, function, home life, carers ## Kidney biopsy ### Will the result change treatment and prognosis ### Bleeding risk, kidney size, blood pressure ### Anticoagulation, platelet count, alternative diagnoses ### A small sample can miss patchy disease ### Chronic scarring mixes with active lesions ### Allocate to light, immunological, electron microscopy ### Give the pathologist timeline and urine findings ## Prescribing and transitions ### Separate loading from maintenance dosing ### Critical illness and circuits change distribution ### Secretion inhibitors raise creatinine without injury ### Haemodynamic fall can still protect long term ### True toxicity hits tubules, interstitium, vessels, crystals ### Staged reintroduction after acute injury ### Final plan states mechanism, trajectory, monitoring