Renal Anatomy, Physiology, and Pathophysiology
Structure and function
Each kidney contains about one million nephrons; the glomerulus filters plasma, and the tubules fine-tune volume, electrolytes, acid-base balance, and waste excretion. The kidney also produces erythropoietin, activates vitamin D, and regulates blood pressure through the renin-angiotensin-aldosterone system. Candidates should connect anatomy to function: glomerular injury causes proteinuria or hematuria, tubular injury causes concentrating and acidification defects, and obstruction causes postrenal injury.
Pathophysiology to recognize
CKD reflects progressive nephron loss with hyperfiltration, proteinuria, fibrosis, and loss of regulatory functions. AKI is classified as prerenal, intrinsic, or postrenal. Prerenal states show sodium avidity and often improve with volume restoration; intrinsic injury may persist despite fluids; postrenal injury requires relief of obstruction. Traps include equating BUN with GFR, assuming oliguria must be present, missing obstruction, and confusing nephrotic with nephritic presentations.
Worked example
A 68-year-old with vomiting, low blood pressure, BUN-to-creatinine ratio above 20:1, low urine sodium, and a rising creatinine improves after isotonic fluid. This pattern suggests prerenal AKI. If creatinine continues to rise and muddy-brown casts appear, intrinsic tubular injury is more likely. Rule of thumb: prerenal physiology is sodium-avid, but diuretics and CKD can blur urine indices, so interpret the whole picture.