Renal disease hypertensive nephropathy

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]. 

Keywords Diabetic nephropathy, renal disease, hypertension, blood pressure, antihypertensive treatment, ACE-1, ARB, dual blockade. 

In the treatment of hypertension, ACE inhibitors are as effective as diuretics, (3-adrenoceptor antagonists, or calcium channel blockers in lowering blood pressure. However, increased survival rates have only been demonstrated for diuretics and (3-adrenoceptor antagonists. ACE inhibitors are approved for monotherapy as well as for combinational regimes. ACE inhibitors are the dtugs of choice for the treatment of hypertension with renal diseases, particularly diabetic nephropathy, because they prevent the progression of renal failure and improve proteinuria more efficiently than the other diugs. 

Patients with renal diseases leading to the nephrotic syndrome often present complex problems in volume management. These patients may exhibit fluid retention in the form of ascites or edema but have reduced plasma volume due to reduced plasma oncotic pressures. This is very often the case in patients with "minimal change" nephropathy. In these patients, diuretic use may cause further reductions in plasma volume that can impair GFR and may lead to orthostatic hypotension. Most other causes of nephrotic syndrome are associated with primary retention of salt and water by the kidney, leading to expanded plasma volume and hypertension despite the low plasma oncotic pressure. In these cases, diuretic therapy may be beneficial in controlling the volume-dependent component of hypertension. 

Vascular cells play a pivotal role in inflammatory renal disease, renal allograft rejection, hypertension, and diabetic nephropathy. However, endothelial and smooth muscle cells are relatively resistant to gene transfer. The only vector that has been reported to... 

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. 

Radiation nephropathy can present in several forms. An acute form is usually seen within a year after radiation and presents with hypertension, anemia and edema. A more insidious chronic form presents primarily with diminished glomerular filtration, hypertension and occasionally proteinuria. When present, associated accelerated hypertension can promote renal failure. Some patients may develop hypertension within several years after radiation but no azotemia. In a subset of patients, mild proteinuria may be the only feature of chronic renal disease [235]. 

Chronic lead nephropathy in moonshiners, more often than not, is accompanied by gout and hypertension, in accord with 19 century descriptions of plumbism and reports from Austraha [1]. A statistically significant odds ratio of 2.4 has been reported for moonshine consumption and end-stage renal disease, suggesting a causal association with lead in fhe absence of symptomatic lead poisoning [31]. 

Lead nephropathy is important because it is one of the few renal diseases that is preventable. Moreover, lead-induced acute renal dysfunction can sometimes be reversed by chelation therapy [19, 28, 63]. The salutary effect of chelation therapy appears to be on the acute reduction in GFR and the acute elevation of blood pressure associated with elevated blood lead concentration rather than on the long-term effects of cumulative exposure associated with endothelial dysfunction, hypertension, and interstitial nephritis. There is no evidence that such therapy reverses established interstitial nephritis. The partial remission achieved among moonshiners and lead workers appears to represent reversal of the physiologic effects of acute poisoning superimposed on chronic lead nephropathy. No improvement in renal function has been observed once advanced interstitial nephritis is present and the steady-state serum creatinine concentration exceeds about 3 mg/ dL [64]. 

In the search for a role for such exposure, the following questions need to be answered (i) does occupational/environmental exposure to a potential nephrotoxic substance play a direct etiological role in the induction of a particular renal disease, (ii) does the exposure correlate with an increased risk for the progression of renal damage already present in patients with glomerulonephritis, diabetic nephropathy, hypertensive renal disease etc. (iii) dobothpossibihties have to be considered concomitantly or separately ... 

End-stage renal disease is treated with dialysis and kidney transplantation. Hypertension and cardiovascular diseases affect the Balkan nephropathy patients less frequently, so they tolerate hemodialysis rather well compared to patients with other renal diseases. The Balkan nephropathy patients on long-term hemodialysis frequenfly develop upper urothelial or urinary bladder carcinoma. 

Proteinuria is a common finding in patients with kidney disease, and the use of a dipstick assay is an important screening test in any patient suspected of having renal disease. Among patients with suspected or proven CKD, including reflux nephropathy and early glomerulonephritis, and those with hypertension or previously detected asymptomatic hematuria, annual urinalysis for proteinuria is accepted as a useful way of identifying patients at risk of... 

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. 

Although not a quantitative measure of renal function, urinary microalbuminuria has been identified as an early marker of renal disease in patients with diabetic nephropathy and numerous other conditions, such as hypertension and obesity. Patients with microalbuminuria (30 to 300 mg/day) on at least two occasions or overt albuminuria (>300 mg/day) should begin to receive pharmacotherapy. For children, microalbuminuria is considered present if albumin excretion exceeds 0.36 mg/kg per day, and overt albuminuria has been defined as an excretion rate that exceeds 4 mg/kg per day. The urinary albumin creatinine ratio is also an accurate predictor of 24-hour proteinuria, a marker of renal disease. Guidelines for monitoring indicate that a urine albumin creatinine ratio of >30 mg/g places the patient at increased risk of developing diabetic nephropathy and is an indication for the initiation of pharmacotherapeutic intervention. Microalbuminuria has also been suggested as a risk factor for renal dysfunction among patients with essential hypertension. ... 

The prevention of urate nephropathy might be a stronger indication because it is irreversible even with proper treatment. Available data indicate, however, that gouty nephropathy is extremely rare in the absence of clinical gout, and evidence that elevation of uric acid by itself may cause renal disease is weak and inconclusive. As discussed previously, renal impairment is very rare in the absence of concurrent hypertension and atherosclerosis. In addition, it is unclear whether uric acid-lowering therapy protects renal function in such individuals. Available data thus do not justify therapy for most patients with asymptomatic hyperuricemia. 

Solvents have been implicated as inducers of glomerulonephritis [72], while the association between chronic interstitial nephritis and analgesic abuse is acknowledged [73] and the association between hypertensive renal disease (nephrosclerosis) and lead nephropathy continues to be explored [74, 75]. According... 

There is also clear evidence that the sequel of lead inducing a chronic nephropathy with hypertension can occur. At times, this hypertension may be sufficiently severe to be malignant and may precipitate an early demise [22]. In more chronic cases, the hypertension may be of moderate degree and not be sufficient to cause progressive deterioration of renal function [43]. However, when confronted with a patient with hypertension and mild renal damage, it can be difficult to determine which came first and particularly difficult to determine whether lead was a contributor to the renal damage that caused the hypertension. In such cases, the hypertensive mechanism would be the same as those associated with other varieties of chronic renal disease. By contrast, many patients with chronic lead nephropathy have demonstrated suppressed plasma renin concentrations indicative of a hyporeninemic hypoaldosteronism [44]. 

A 67-year-old man with end-stage renal disease secondary to hypertensive nephropathy developed a herpes zoster infection and was given oral valaciclovir 1 g/day. After 5 days, he complained of hallucinations. Valaciclovir was withdrawn and peritoneal diatysis was continued. The serum aciclovir concentration on admission was 20 mg/1 and fell to 0.7 mg/1 by day 7, when his symptoms had completely resolved. 

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