Renal Transplantation and Renal Physiology
Renal physiology
GFR is roughly 125 mL per minute; creatinine is a convenient but imperfect marker, influenced by muscle mass and delayed in rise. Autoregulation and tubuloglomerular feedback stabilise glomerular filtration. Diuretic sites: acetazolamide in the proximal tubule, loop diuretics in the thick ascending limb, thiazides in the distal convoluted tubule, spironolactone in the collecting duct. Understand sodium handling, potassium shifts, acid-base regulation, and ADH action.
Transplantation
Candidates are evaluated for cardiac risk and infection; donors may be living or deceased. Induction therapy is followed by maintenance with a calcineurin inhibitor, antimetabolite, and steroid. Rejection types: hyperacute from preformed antibodies; acute cellular, treated with steroids; antibody-mediated, treated with plasmapheresis and immunoglobulin; chronic, with progressive fibrosis.
Complications
Delayed graft function requires distinguishing acute tubular necrosis from rejection, obstruction, urine leak, and drug toxicity. Vascular thrombosis occurs early. Ureteral stenosis and lymphocele present with rising creatinine or hydronephrosis. BK virus nephropathy mimics rejection and is managed by reducing immunosuppression.
Traps
Attributing every creatinine rise to rejection; forgetting BK virus; overlooking recurrent disease such as FSGS; ignoring drug levels and nephrotoxicity.
Worked example
A transplant recipient with rising creatinine on day five needs Doppler ultrasound and exclusion of obstruction or leak before a biopsy is labelled rejection.