Acute injury, chronic disease and hypertension
Acute kidney injury is a change over time, so establish a credible baseline and the timing of both creatinine and urine-output changes. Volume depletion, impaired perfusion, tubular injury, glomerular disease, interstitial inflammation and obstruction may coexist. Medication review is central. A combination of reduced effective circulation, diuretics, renin-angiotensin blockade and nonsteroidal anti-inflammatory exposure can impair adaptive hemodynamics without every component causing the same lesion.
Urinalysis and microscopy can localize an injury. Coarse granular casts and tubular epithelial cells support tubular injury. Dysmorphic erythrocytes and erythrocyte casts suggest glomerular inflammation. White-cell casts can occur in interstitial or upper urinary tract inflammation and are not specific to one diagnosis. Fractional excretion indices are contextual aids: diuretics, sepsis, chronic kidney disease and other factors limit rigid cutoffs. Renal imaging addresses obstruction and structural questions, but hydronephrosis has its own differential and is not a substitute for the complete assessment.
Chronic kidney disease requires evidence of persistent structural or functional abnormality, generally over at least three months. Classify filtration and albuminuria separately, establish the likely cause and assess the trajectory. One abnormal result during an acute illness is insufficient to reconstruct chronicity. Estimated filtration is not a direct measure of symptoms, nutrition or readiness for dialysis, and risk can differ markedly between patients with the same filtration category.
Protective treatment is tailored to the underlying disease and tolerability. Blood pressure management, appropriate renin-angiotensin system therapy, sodium-glucose cotransporter inhibitors and selected additional agents have roles in eligible patients. Monitor kidney function, potassium, volume and relevant adverse effects. An initial modest hemodynamic filtration change does not necessarily mean permanent injury, but severe changes or concurrent illness need assessment. Anemia evaluation includes iron status and alternative causes; normalizing hemoglobin with an erythropoiesis-stimulating agent is not a universal therapeutic goal.
For hypertension, first verify measurement technique, adherence, medication exposures and out-of-office readings. An apparent resistant pattern can reflect inaccurate measurement or inadequate therapy. Hypokalemia with suppressed renin raises a different diagnostic question from renal artery disease or episodic catecholamine symptoms. Adrenal imaging does not reliably establish which gland produces aldosterone. Emergency treatment is driven by acute target-organ injury and clinical context rather than an isolated high number without assessment.