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

A reversible lysozymuria indicative of proximal tubular damage to the kidney was found in three out of five patients with diabetic ketosis, and a persistent lysozymuria was found in many patients with diabetic nephropathy. There was no relation between lysozymuria and the degree of proteinuria, and lysozymuria was not due to urinary tract infection. The degree of lysozymuria could be used to assess the severity of diabetic nephropathy.
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PMID:Lysozymuria in diabetes. 125 52

Geographic/population variation in the prevalence of diabetic nephropathy is well recognised. In a study of 'native' Indians, we screened 102 non-proteinuric diabetes mellitus patients (64 NIDDM, 38 IDDM; mean age and diabetic duration 48.7 and 6.5 years, 21.6 and 6.2 years, respectively) with blood pressure less than or equal to 170/105 and without congestive heart failure, ketonuria or urinary tract infection, for the presence of microalbuminuria (albumin excretion rate greater than 20 micrograms/min). Fifty-six patients (34 NIDDM, 22 IDDM) also underwent detailed fundus examination. Seventeen NIDDM (26.6%) and 3 IDDM (7.9%) patients had microalbuminuria. Glycated hemoglobin was significantly higher in microalbuminurics in the NIDDM group (P less than 0.05). Diabetic retinopathy tended to occur more frequently in microalbuminurics (NIDDM and IDDM).
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PMID:The prevalence of microalbuminuria in diabetes: a study from north India. 187 3

Renal papillary necrosis in 4 diabetic patients is described. Two of them had underlying diabetic nephropathy. Urinary tract infection was present in all of them. Three patients had passed fleshy material in the urine while in one the diagnosis was established by excretory urography. Two patients required haemodialysis for acute renal failure caused by sloughed papillae. The condition should be suspected in diabetic subjects who develop recurrent episodes of urinary tract infection, renal colic, haematuria or obstructive uropathy.
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PMID:Renal papillary necrosis in diabetes mellitus. 209 26

Although diabetes mellitus is reported in 29% of patients with renal papillary necrosis (RPN), the frequency of RPN among patients with insulin-dependent diabetes mellitus (IDDM) has from autopsy studies been estimated to be only 4.4%. In vivo data on the prevalence of RPN in patients with IDDM have been lacking. We therefore studied the prevalence of RPN in 76 patients with long-standing IDDM and in 34 age-matched control subjects by intravenous urography. None of the control subjects showed radiographic signs of papillary necrosis. RPN was observed in 18 patients (23.7%); 15 were women (83.3%). Age and duration of diabetes was not different between patients with and without papillary necrosis, and there was no significant difference between the two groups regarding the prevalence of microangiopathic complications, i.e., proliferative retinopathy and diabetic nephropathy. Microscopic hematuria was three times more frequent in patients with than without RPN (44 vs. 16%; P less than .02). In addition, pyuria was reported in 40% of patients with papillary necrosis, and 61% of them gave a positive history of urinary tract infection compared to 16% (P less than 05) and 32% (P less than .02), respectively, in patients without papillary necrosis. It is concluded that RPN is a more frequent complication of long-standing IDDM than appreciated from autopsy studies, and being female and having a history of urinary tract infection are associated with an increased risk of RPN.
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PMID:Renal papillary necrosis in patients with IDDM. 270 11

Altered urinary excretion of glycosaminoglycans (GAG) has been reported in patients with nephrolithiasis, with chronic glomerulonephritis, and incipient diabetic nephropathy, but evaluation of urinary GAG has not been reported in infections and proliferating diseases of the urinary tract. Urinary excretion of GAG was measured in 50 patients with idiopathic calcium nephrolithiasis (ICN) of whom 20 had associated urinary tract infection, in 20 subjects with recurrent infection of the urinary tract (UTI), and in 18 patients with bladder papillomatosis. Mean values were significantly lower in ICN, increased in papillomatosis, and in the normal range in UTI.
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PMID:Urinary excretion of glycosaminoglycans in urological disease. 343 40

We have evaluated the incidence, prevalence, predisposing factors and evolution of urinary tract infection (UTI) developing late after transplantation in 63 patients whose graft had lasted at least 3 months and whose follow-up averaged 7 years. Beyond 3 months after transplantation incidence of UTI decreases progressively, from 25 to 0%, 50% of the patients remaining free of infection throughout the period of observation. Neither the original kidney disease except perhaps diabetic nephropathy nor the presence of vesicoureteral reflux were predisposing factors. Incidence and prevalence in females were twice that in male. Late UTI did not affect graft or patient survival, or graft function at 5 years. Most UTI were asymptomatic and had a benign course. However, in 3 patients septicemia or graft dysfunction ensued demonstrating the need for continuous monitoring of urine cultures.
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PMID:Late urinary tract infection after transplantation: prevalence, predisposition and morbidity. 388 73

We studied 182 patients with chronic renal failure by urinalysis and urine cultures. Of the patients 27 per cent had significant bacteriuria (more than 10(5) per ml.), 38 per cent had significant pyuria (more than 10 white blood cells per high power field), 19 per cent had urinary tract infection and 7 per cent had symptomatic urinary tract infection. All 12 patients with symptomatic urinary tract infection had significant bacteriuria and 11 had significant pyuria, while 1 had 5 to 10 white blood cells per high power field. Incidences of urinary tract infection differed depending on the primary renal disease (12, 13, 41 and 67 per cent for chronic glomerulonephritis, diabetic nephropathy, polycystic kidney and chronic pyelonephritis, respectively). Among the patients with chronic glomerulonephritis no significant differences were seen in frequencies of bacteriuria and urinary tract infection between male and female patients or between those who did and did not undergo hemodialysis. Also, no significant correlation was seen between bacteriuria and daily urine output but pyuria was significantly more frequent in oliguric patients or those on hemodialysis.
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PMID:Urinary tract infection in oliguric patients with chronic renal failure. 399 25

Nephropathy may develop in patients with type 1 diabetes because poor glycemic control produces effects that eventually lead to glomerular scarring and renal failure. The worse and more prolonged the hyperglycemia, the greater the risk of diabetic nephropathy. In patients with type 2 diabetes, hyperglycemia, as well as insulin resistance and generalized vascular disease, is involved in the pathogenesis of nephropathy. The glomerular changes of early diabetic nephropathy can be identified only by renal biopsy or by testing for microalbuminuria. Once macroalbuminuria occurs (albumin excretion rate, > 300 mg/day), usually after type 1 diabetes has been present for 10 to 15 postpubertal years, end-stage renal disease is almost inevitable. However, aggressive control of hypertension in diabetic patients without microalbuminuria helps avoid nephropathy, and tight glycemic control in those with microalbuminuria can avoid or delay its onset. Even when macroalbuminuria is present, treatment can prolong renal function. Aggressive antihypertensive therapy, especially with ACE inhibitors, can reduce renal decline by half. Avoiding circumstances that may damage the kidneys (e.g., use of radiocontrast materials or nephrotoxic drugs, dehydration, hyperlipidemia, urinary tract infection, buildup of AGEs) is critical. Some treatment methods are controversial (dietary protein restriction) or still under investigation (use of injected or oral heparin) but may help delay renal transplantation or dialysis.
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PMID:Dealing with diabetic nephropathy. 1002 5

Low-protein diet decreases hyperfiltration and albuminuria, and slows down the decrease in glomerular filtration in diabetic patients with incipient diabetic nephropathy (DN). The patients with incipient DN are recommended to intake 0.6-0.8 g of proteins per kg of body weight with a sufficient amount of essential amino acids. A high occurrence of urologic infections was found in risk groups of diabetic patients, namely in those with ketoacidosis, urinary bladder dysfunction in urogenital forms of autoimmune neuropathy, and in pregnant diabetic patients. Each symptomatic infection of renal parenchyma and urinary tract should be urgently treated. The cases with relapses of urinary tract infection should be subdued to a long-term prophylactic antimicrobial treatment.
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PMID:[Diabetic nephropathy]. 1121 52

We present a 77-year-old male with moderate chronic renal insufficiency from diabetic nephropathy who developed severe metabolic acidosis and life threatening hyperkalemia on treatment with regular dose of trimethoprim-sulfamethoxazole (TMP-SMZ) for urinary tract infection. The metabolic acidosis and hyperkalemia resolved upon appropriate medical intervention and discontinuation of TMP-SMZ. While hyperkalemia has commonly been reported with high dose of TMP-SMZ, severe metabolic acidosis is quite uncommon with regular dose TMP-SMZ. We emphasize that patients with renal tubular acidosis (RTA), renal insufficiency, aldosterone deficiency, old age with reduced renal mass and function, and angiotensin converting enzyme (ACE)-inhibitor therapy are at high risk of developing these severe and potentially life threatening complications.
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PMID:Life threatening hyperkalemia and acidosis secondary to trimethoprim-sulfamethoxazole treatment. 1173 Feb 76


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