Kidney disease diabetic nephropathy

Among the various primary and secondary glomerular diseases, diabetic nephropathy represents the most common cause of stage 5 chronic kidney disease accounting for about 44% of all patients on dialysis. One important mediator of glomerular injury in diabetic... 

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Diabetes is the most frequent cause of end-stage renal disease. Hypertension, which is common among patients with type 2 diabetes, accelerates the development and progression of renal disease. Early and tight blood pressure control in diabetic patients, preferably with antihypertensive agents that have proven reno-protective properties, is therefore essential to minimize loss of kidney function. Several controlled clinical trials have investigated and proved the beneficial effects of ARBs on type 2 diabetic nephropathy [10-14]. 

ACE-inhibitors may be considered as first-choice therapy in patients with all forms of primary hypertension, but they are preferred in hypertension associated with heart failure, reduced systolic left ventricular ejection fraction or diabetic nephropathy, previous MI or stroke, chronic kidney disease and patients with high coronary disease risk, based on the compelling evidence of the efficacy of these drugs in such patient populations [8]. 

In type 1 diabetes, diabetic nephropathy follows a predictable course from onset of diabetes to the onset of microalbuminuria to frank nephropathy to end-stage renal disease or death. Microalbuminuria (a tiny amount of protein in the urine) develops 10-14 years after onset of diabetes. Without treatment, clinical nephropathy follows within 5 years, and severe renal impairment leading to end-stage renal failure develops approximately 5 years later. Hypertension develops in association with microalbuminuria and progresses with diabetic nephropathy, further damaging the kidneys. Once end-stage renal disease (ESRD) is reached, the toxins in the body can no longer be cleared by the kidneys and, unless treated by dialysis, can build up to fatal levels. 

It is not known whether these changes are the result of a normal aging process (i.e., involutional) or the result of the interplay of pathology and age. Cumulative exposure to common causes of chronic kidney disease (CKD), such as (1) atherosclerosis, (2) hypertension, (3) heart failure, (4) diabetes,(5) obstructive nephropathy, (5) infection, (6) immune insult, (7) nephrotoxins such as lead, and (8) dietary protein increases with age and it is difficult to separate these effects from those of healthy aging. The decline in GFR with increasing age may be largely attributable to hypertension, atherosclerosis, or heart failure. In the absence of these or other identifiable causes of kidney disease, many older subjects have stable GFR over time. 

Diseases of the kidney that are discussed in this section include (1) the uremic syndrome, (2) chronic kidney disease, (3) end-stage renal disease, (4) diabetic nephropathy, (5) hypertensive nephropathy, (6) glomerular diseases, (7) interstitial nephritis, (8) polycystic Iddney disease, (9) polycystic kidney disease, (10) toxic nephropathy, (11) obstructive uropathy, (12) tubular diseases, (13) renal calculi, and (14) cystinuria. In addition, this section also includes discussions on (1) prostaglandins and NS AIDS in kidney disease, (2) monoclonal light chains and kidney disease, and (3) urinary osmolality. 

Ehe-existent kidney disease, particularly diabetic nephropathy with renal insufficiency, is the major risk factor. Conditions associated with decreased renal blood flow, including congestive heart failure and dehydration, also confer risk. The presence of multiple myeloma has been considered a relative contraindication for contrast use, but the risk appears to be associated with concomitant dehydration, renal insufficiency, or hypercalcemia rather than the diagnosis itself. Both... 

The incidence of ACEI- or angiotensin II receptor blocker (ARB)-mediated renal failure has not been established. However, patients with severe atherosclerotic renal artery stenosis, those hospitalized with congestive heart failure, and those with chronic kidney disease, including diabetic nephropathy, are most likely to experience a significant decline in renal function with these agents. 

It has been clearly recognized that one of the clinical hallmarks of diabetic nephropathy is proteinuria in excess of 500 mg/24 hours this can be easily detected by urine dipstick testing, which has a detection limit of 150-200 mg/liter of albumin. Such clinical proteinuria portends a progressive decline in kidney function leading to end-stage renal failure over an average 7-year period. This clinical proteinuria is not sudden but is preceded by years of microalbuminuria. Thus microalbuminuria represents an early manifestation of diabetic kidney disease. In fact, 6-20% of patients with IDDM present with microalbuminuria. Left uncontrolled, albumin excretion in microalbuminuric subjects can increase at the rate of 7-18.6% per year. 

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