Urine Nephrology Now: A Primer for Students in Nephrology
AIN represents a common cause of acute kidney injury, particularly in hospitalized patients. Understanding the causes, recognition, and management is essential for nephrology practice.
The most common cause of AIN in clinical practice involves hypersensitivity reactions to medications. NSAIDs represent the leading cause, followed by antibiotics (particularly penicillins, sulfonamides, and fluoroquinolones) and proton pump inhibitors.
The classic triad of fever, rash, and eosinophilia occurs in less than 10% of patients. Most patients present with nonspecific acute kidney injury. Maintain high index of suspicion based on temporal relationship to medication exposure.
Diagnosis relies on clinical suspicion, temporal relationship to drug exposure, and exclusion of other causes. Urinalysis may show white blood cell casts, eosinophiluria, and sterile pyuria. Kidney biopsy provides definitive diagnosis but is rarely necessary.
Immediate discontinuation of the offending agent represents the most important intervention. Corticosteroids may be beneficial if started early, particularly for severe cases or when AIN is diagnosed within weeks of onset.
Chronic use of analgesic combinations, particularly those containing phenacetin, can lead to chronic tubulointerstitial nephritis. Modern analgesic nephropathy is less common but can still occur with chronic NSAID use.
Chronic lithium therapy can cause diabetes insipidus and chronic tubulointerstitial nephritis. Regular monitoring of kidney function is essential in patients receiving lithium therapy.
Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disease. Caused by mutations in PKD1 (85%) or PKD2 (15%) genes, leading to progressive cyst development and kidney enlargement.
Hereditary nephritis caused by mutations in type IV collagen genes. Characterized by progressive nephritis, sensorineural hearing loss, and ocular abnormalities. More severe in males, leading to end-stage renal disease by age 30 in classic forms.
Inherited tubulopathy affecting the thick ascending limb due to mutations in sodium-potassium-chloride cotransporter or associated channels. Characterized by hypokalemia, metabolic alkalosis, hyperreninemia, and normal blood pressure.
Caused by mutations in thiazide-sensitive sodium-chloride cotransporter in distal tubule. Features include hypokalemia, metabolic alkalosis, hypomagnesemia, hypocalciuria, and normal blood pressure. Generally milder than Bartter syndrome.
Generalized dysfunction of proximal tubule resulting in impaired reabsorption of glucose, amino acids, phosphate, bicarbonate, and low-molecular-weight proteins. Can be inherited or acquired from various causes including medications and heavy metals.