diabetic nephropathy diabetic nephropathy diabetic nephropathy, also known as diabetic kidney disease, is the chronic loss of kidney function occurring in those with diabetes mellitus. diabetic nephropathy is the leading causes of chronic kidney disease (ckd) and end-stage renal disease (esrd) globally. the triad of protein leaking into the urine (proteinuria or albuminuria), rising blood pressure with hypertension and then falling renal function is common to many forms of ckd. protein loss in the urine due to damage of the glomeruli may become massive, and cause a low serum albumin with resulting generalized body swelling (edema) so called nephrotic syndrome. likewise, the estimated glomerular filtration rate (egfr) may progressively fall from a normal of over 90 ml/min/1.73m2 to less than 15, at which point the patient is said to have end-stage renal disease. it usually is slowly progressive over years. diabetic nephropathyother namesdiabetic kidney diseasetwo glomeruli in diabetic nephropathy: the acellular light purple areas within the capillary tufts are the destructive mesangial matrix deposits.specialtynephrology, endocrinology symptomsalbuminuria, peripheral edema, high blood pressure, tirednessrisk factorshigh blood pressure, tobacco smoking, unstable blood glucosediagnostic methodabnormal levels of urinary albuminpreventionsmoking cessationtreatmentace inhibitors pathophysiologic abnormalities in diabetic nephropathy usually begin with long-standing poorly controlled blood glucose levels. this is followed by multiple changes in the filtration units of the kidneys, the nephrons. (there are normally about 750,000–1.5 million nephrons in each adult kidney). initially, there is constriction of the efferent arterioles and dilation of afferent arterioles, with resulting glomerular capillary hypertension and hyperfiltration particularly as nephrons become obsolescent and the adaption of hyperfiltration paradoxically causes further shear stress related damage to the delicate glomerular capillaries, further proteinuria, rising blood pressure and a vicious circle of additional nephron damage and decline in overall renal function. concurrently, there are changes within the glomerulus itself: these include a thickening of the basement membrane, a widening of the slit membranes of the podocytes, an increase in the number of mesangial cells, and an increase in mesangial matrix. this matrix invades the glomerular capillaries and produces deposits called kimmelstiel-wilson nodules. the mesangial cells and matrix can progressively expand and consume the entire glomerulus, shutting off filtration. the status of diabetic nephropathy may be monitored by measuring two values: the amount of protein in the urine - proteinuria; and a blood test called the serum creatinine. the amount of the proteinuria reflects the degree of damage to any still-functioning glomeruli. the value of the serum creatinine can be used to calculate the estimated glomerular filtration rate (egfr), which reflects the percentage of glomeruli which are no longer filtering the blood. treatment with an angiotensin converting enzyme inhibitor or angiotensin receptor blocker, which dilates the arteriole exiting the glomerulus, thus reducing the blood pressure within the glomerular capillaries, which may slow (but not stop) progression of the disease. three classes of diabetes medications – glp-1 agonists, dpp-4 inhibitors, and sglt2 inhibitors– are also thought to slow the progression of diabetic nephropathy. diabetic nephropathy is the most common cause of end-stage renal disease and is a serious complication that affects approximately one quarter of adults with diabetes in the united states. affected individuals with end-stage kidney disease often require hemodialysis and eventually kidney transplantation to replace the failed kidney function. diabetic nephropathy is associated with an increased risk of death in general, particularly from cardiovascular disease. signs and symptoms the onset of symptoms is 5 to 10 years after the disease begins. a usual first symptom is frequent urination at night: nocturia. other symptoms include tiredness, headaches, a general feeling of illness, nausea, vomiting, frequent daytime urination, lack of appetite, itchy skin, and leg swelling. the clinical presentation of diabetic nephropathy (dn) is characterized by proteinuria (protein in the urine), hypertension and progressive loss of kidney function. the process may be initially indolent, making regular screening for diabetic nephropathy in patients with diabetes mellitus of great importance. risk factors not all patients with diabetes go on to develop diabetic nephropathy. the main risk factors that increase the likelihood of developing diabetic nephropathy are: poor control of blood glucose uncontrolled high blood pressure type 1 diabetes mellitus, with onset before age 20 past or current cigarette use a family history of diabetic nephropathy- certain genes have been identified that are associated with dn. ( however, no direct correlation has been established yet. one of these genes is apol1, which has been found to be associated with nephropathy in african american individuals.) certain racial groups (african americans, mexican americans, and pima indians are at higher risk). pathophysiology diagram showing the basic outline of nephron structure and function: diabetic nephropathy is associated with changes in the afferent and efferent arterioles, causing capillary hypertension; and damage to the glomerular capillaries of multiple causes, including mesangial matrix deposition