Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011881 (diabetic nephropathy)
 10,836 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diabetic nephropathy leading to end stage renal failure with 30 to 40% cumulative incidence remains one of the great life threatening dangers for type I diabetics. Its natural history gets its impact due to the biochemical sequela of diabetic hyperglycemia such as polyol accumulation or glycation processes. Functional changes may be detected by microalbuminuria which in turn is followed by intraglomerular, intrarenal and finally systemic hypertension. Hypertension itself seems to be part of the self perpetuating process, and therefore antihypertensive treatment has been shown to be an effective area. Antihypertensive treatment by itself is effective in the slowing down of the decline of glomerular filtration rate, together with decreasing the amount of albumin excretion and, therefore, might be expected to be of value in prolonging the renal prognosis over a length of time. From the theoretical point of view the ACE inhibitors were looked upon as beneficial and therefore preferable as interventional tools because of their special effects of blood pressure redistribution within the glomeruli. Long term reports and a lot of short and intermediate term controlled studies were able to confirm the expected effects. Whether this is the case also in borderline hypertension or even in normotensive diabetics remains finally to be established. The question of long term effects such as survival rates and the superiority of antihypertensive treatments with beta blockers or drug combinations, or whether these results reflect merely their systemic blood pressure lowering effects remain finally to be elucidated.
 ...
PMID:Effects of ACE-inhibitors in hypertensive and normotensive diabetic patients with diabetic nephropathie. 220 29

Serum creatinine levels were determined prospectively every 2 to 3 months in 40 patients with diabetic nephropathy for a global observation period of 864 months. The monthly creatinine increasing rate was significantly lower in normotensive periods, mean arterial pressure (MAP) less than 115 mmHg, when compared with hypertensive periods, MAP greater than 125 mmHg. No significant difference was shown in periods with borderline hypertension (MAP between 115-124 mmHg). The mean creatinine increases were of 0.036 mg/dl/month, 0.3 mg/dl/month and 0.046 mg/dl/month respectively. Normotension was associated with a slowing down of the rate of decline in renal function in this group of moderate kidney failure with an initial mean serum creatinine of 2.26 mg/dl. The exposure of patients to nephrotoxics (aminoglycosides, and possibly anesthesia) significantly accelerated the decline in renal function: 0.39 mg/dl/month and 0.17 mg/dl/month respectively according to the concomitance or not of toxics and hypertension. The reported protective effect of diabetes against aminoglycosides nephrotoxicity in experimental conditions was not reflected in our clinical results. On the contrary, we suggest a possible enhanced sensibility of the diabetic patient with diabetic nephropathy to aminoglycosides leading to an acceleration of the progression of renal failure.
 ...
PMID:Hypertension and nephrotoxicity in the rate of decline in kidney function in diabetic nephropathy. 381 4

Alterations in the renal dopamine [DA] system have been suggested to contribute to the development of hypertension and diabetic nephropathy. To identify early abnormalities in renal handling of DA and sodium we challenged 16 normotensive patients with uncomplicated insulin-dependent diabetes (IDDM), 18 normotensive nondiabetic subjects with familial borderline hypertension, and 16 healthy controls, 14-29 years old, with a high-sodium diet (HSD). Systolic blood pressure was slightly higher in subjects with familial borderline hypertension than in the other groups on a normal sodium diet (NSD) (P < 0.05). Blood pressure and 24-h urinary measurements were performed on a NSD and after 3 days on a HSD. Twenty-four-hour urinary DA excretion was similar in all groups on NSD. A significant rise in DA excretion was noted after HSD in control subjects (P < 0.01), but not in subjects with a family history of hypertension or with IDDM. Urinary sodium excretion increased in all groups. A correlation between the change in DA and sodium/creatinine ratio after HSD was seen in healthy controls (r = 0.57, P = 0.02) but not in those with familial borderline hypertension (r = 0.18, P = 0.47) or with IDDM (r = 0.40, P = 0.15). A rise in systolic (but not diastolic) pressure was noted only in the IDDM group after HSD (P = 0.02). In conclusion, an impairment in the renal DA and sodium system can be detected early in IDDM and in individuals with familial hypertension. We speculate that this impairment may contribute to the development of hypertension and microvascular disease in both conditions.
 ...
PMID:The dopaminuric response to high salt diet in insulin-dependent diabetes mellitus and in family history of hypertension. 909 Jun 56