Utility of Urinary Biomarkers in Kidney Transplant Function Assessment

Kidney may undertake normal function immediately after transplantation or even several or over a dozen days delay. Absence of normal renal transplant function may lead to acute kidney injury (AKI), nephrotic syndrome (NS) and chronic kidney disease (CKD). Acute kidney injury (AKI) is characterized functionally by a rapid decline in the glomerular filtration rate (GFR), and biochemically by the resultant accumulation of nitrogenous wastes such as bloodurea nitrogen and creatinine (Devarajan, 2010). Nephrotic syndrome (NS) is a nonspecific disorder in which the kidneys damage is accompanied by a leak of large amounts of protein (proteinuria at least 3.5 grams per day per 1.73m2 body surface area) from the blood into the urine. Nephrotic syndrome is a disorder of the glomerular filtration barrier. The multiprotein complex between adjacent podocyte foot processes the slit diaphragm, is essential to the control of the actin cytoskeleton and cell morphology. Signaling from slit diaphragm proteins to the actin cytoskeleton is mediated via the Rho GTP-ases. These are thought to be involved in the control of podocyte motility, which has been postulated as a focus of proteinuric pathways (Hull & Goldsmith, 2008). It is common belief that nephrotic syndrome after transplantation results mainly from recurrence of renal disease in transplanted kidney and not defective graft function. Chronic kidney disease (CKD) – it is kidney damage for ≥3 months, defined by structural or functional abnormalities of the kidney, with or without decreased GFR, manifested by either pathological abnormalities or markers of kidney damage, including abnormalities of blood or urine or abnormalities in imaging tests (Ahmad et al., 2006).