Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mesalazine is a first-line drug in pediatric inflammatory bowel disease, and is effective as primary treatment and maintenance therapy. It's usually well tolerated, but various side effects have been described. A 15-year-old female with ulcerative colitis developed polyuria, polydipsia, vomiting, and fatigue. She was receiving mesalazine (500 mg, thrice daily, p.o.) and prednisolone for 4 months. She was detected as acute tubular injury as she had dehydration, acidosis, hypostenuria, hematuria, proteinuria, low levels of potassium, uric acid and bicarbonate. These findings were attributed to interstitial nephritis as a side effect of mesalazine, however as renal biopsy was disapproved by the parents, it was not confirmed. After discontinuation of mesalazine her renal tubular functions improved. Potassium and phosphorus supplements were stopped after 7 months, although she had to continue bicarbonate supplementation. We conclude that regular renal screening is important in patients receiving 5-ASA therapy to prevent rare but serious complications, such as interstitial nephritis sometimes leading to chronic renal failure.
 ...
PMID:Acute tubular injury associated with mesalazine therapy in an adolescent girl with inflammatory bowel disease. 1740 67

Glomerular polycystic kidney disease was diagnosed in an 11 month old, female, Blue Merle Collie. Clinical signs (polyuria, polydipsia, vomiting, diarrhea, partial anorexia) and laboratory work (blood urea nitrogen, creatinine, serum phosphorus, specific gravity, proteinuria, nonregenerative anemia) indicated chronic renal failure.However, after the study of a biopsy specimen, a definitive diagnosis was reached and the prognosis was determined. Necropsy findings and histopathological studies revealed: presence of glomerular cysts, atrophy of glomerular tufts and sclerosis of the interstitial tissue.
 ...
PMID:Glomerular polycystic kidney disease in a dog (blue merle collie). 1742 9

Dietary manipulation, including protein, phosphorus, and sodium restriction, when coupled with the vegetarian nature of the renal diet and ketoacid supplementation can potentially exert a cardiovascular protective effect in chronic renal failure patients by acting on both traditional and nontraditional cardiovascular risk factors. Blood pressure control may be favored by the reduction of sodium intake and by the vegetarian nature of the diet, which is very important also for lowering serum cholesterol and improving plasma lipid profile. The low protein and phosphorus intake has a crucial role for reducing proteinuria and preventing and reversing hyperphosphatemia and secondary hyperparathyroidism, which are major causes of the vascular calcifications, cardiac damage, and mortality risk of uremic patients. The reduction of nitrogenous waste products and lowering of serum PTH levels may also help ameliorate insulin sensitivity and metabolic control in diabetic patients, as well as increase the responsiveness to erythropoietin therapy, thus allowing greater control of anemia. Protein-restricted diets may have also anti-inflammatory and anti-oxidant properties. Thus, putting aside the still debatable effects on the progression of renal disease and the more admitted effects on uremic signs and symptoms, it is possible that a proper nutritional treatment early in the course of renal disease may be useful also to reduce the cardiovascular risk in the renal patient. However, conclusive data cannot yet be drawn because quality studies are lacking in this field; future studies should be planned to assess the effect of renal diets on hard outcomes, as cardiovascular events or mortality.
 ...
PMID:Potential benefits of renal diets on cardiovascular risk factors in chronic kidney disease patients. 1765 13

Chronic renal failure (CRF) is one of the most common illnesses of geriatric cats. Common clinical signs include polydipsia, polyuria, decreased appetite, weight loss, and vomiting. Although CRF is incurable, it may be possible to delay the progression of the disorder by feeding an appropriate diet and by monitoring and normalizing (if possible) several parameters, including blood pressure, serum phosphorus and potassium levels, parathyroid hormone levels, and proteinuria.
 ...
PMID:Feline chronic renal failure: long-term medical management. 1772 88

Intrauterine growth restriction (IUGR) has been shown to influence renal development and lead to fewer nephrons. Data on long term renal function after IUGR are limited. We studied the effect on renal function of IUGR in aging rats. IUGR was induced using a model of bilateral uterine artery ligation in pregnant Wistar rats. Renal function was studied at the age of 18 months. In male IUGR rats, estimated glomerular filtration rate was significantly decreased compared to male control rats [1.1 (SD 0.3) 1.7 (SD 0.3) ml x min(-1), p<0.05]. Female IUGR rats showed an increased urinary protein excretion compared with female control rats [84 (SD 73) vs. 12 (SD 13) mg x 24h(-1), p<0.01]. All male rats showed heavy proteinuria (p<0.01 vs. female rats from same experimental group), with no significant differences between the groups. Tubular reabsorption of phosphorus was lower in females, but showed no differences between the experimental groups. In conclusion, IUGR impairs renal function in the rat. It is suggested that a low nephron endowment leads to proteinuria as a sign of glomerular damage, and ends with a decrease in glomerular filtration rate as a sign of glomerular loss.
 ...
PMID:Influence of intrauterine growth restriction on renal function in the adult rat. 1830 77

Childhood chronic kidney disease commonly progresses toward end-stage renal failure, largely independent of the underlying disorder, once a critical impairment of renal function has occurred. Hypertension and proteinuria are the most important independent risk factors for renal disease progression. Therefore, current therapeutic strategies to prevent progression aim at controlling blood pressure and reducing urinary protein excretion. Renin-angiotensin-system (RAS) antagonists preserve kidney function not only by lowering blood pressure but also by their antiproteinuric, antifibrotic, and anti-inflammatory properties. Intensified blood pressure control, probably aiming for a target blood pressure below the 75th percentile, may exert additional renoprotective effects. Other factors contributing in a multifactorial manner to renal disease progression include dyslipidemia, anemia, and disorders of mineral metabolism. Measures to preserve renal function should therefore also comprise the maintenance of hemoglobin, serum lipid, and calcium-phosphorus ion product levels in the normal range.
 ...
PMID:Therapeutic strategies to slow chronic kidney disease progression. 1833 52

Tenofovir disoproxil fumarate (TDF) is a first-line drug used in patients with highly active retroviral disease; however, it can cause renal failure associated with many tubular anomalies that may be due to down regulation of a variety of ion transporters. Because rosiglitazone, a peroxisome proliferator-activated receptor-gamma agonist induces the expression of many of these same transporters, we tested if the nephrotoxicity can be ameliorated by its use. High doses of TDF caused severe renal failure in rats accompanied by a reduction in endothelial nitric-oxide synthase and intense renal vasoconstriction; all of which were significantly improved by rosiglitazone treatment. Low-dose TDF did not alter glomerular filtration rate but produced significant phosphaturia, proximal tubular acidosis, polyuria and a reduced urinary concentrating ability. These alterations were caused by specific downregulation of the sodium-phosphorus cotransporter, sodium/hydrogen exchanger 3 and aquaporin 2. A Fanconi's-like syndrome was ruled out as there was no proteinuria or glycosuria. Rosiglitazone reversed TDF-induced tubular nephrotoxicity, normalized urinary biochemical parameters and membrane transporter protein expression. These studies suggest that rosiglitazone treatment might be useful in patients presenting with TFV-induced nephrotoxicity especially in those with hypophosphatemia or reduced glomerular filtration rate.
 ...
PMID:Rosiglitazone reverses tenofovir-induced nephrotoxicity. 1856 54

In beta-thalassemia, profound anemia and severe hemosiderosis cause functional and physiological abnormalities in various organ systems. In recent years, there have been few published studies demonstrating proteinuria, aminoaciduria, low urine osmolality, and excess secretion of the tubular damage markers, such as urinary N-acetyl-D-glucosaminidase (U(NAG)) and beta2 microglobulin, in patients with thalassemia. The object of this study was to analyze renal tubular and glomerular function in pediatric patients with beta-thalassemia and to correlate the renal findings to iron overload. Thirty-seven patients with beta-thalassemia major and 11 with thalassemia intermedia were studied. Twelve children without iron metabolism disorders or renal diseases served as a control group. No difference in blood urea nitrogen (BUN), serum creatinine, creatinine clearance, electrolytes, fractional excretion of sodium and potassium, and tubular phosphorus reabsorption was found. Serum uric acid was equal in the two groups, but its urine excretion was significantly higher in the thalassemic group. U(NAG) and U(NAG) to creatinine ratio (U(NAG/CR)) were elevated in all patients with thalassemia compared with the control group (p < 0.001) and were directly correlated to the amount of transfused iron but not to actual ferritin level. We found that renal tubular function is impaired in children with beta- thalassemia major and intermedia. It is not known whether these functional abnormalities would have any long-term effects on the patients. Further studies are needed, and means of preventing these disturbances should be sought.
 ...
PMID:Renal function in children with beta-thalassemia major and thalassemia intermedia. 1858 Nov 45

The high estimated prevalence of chronic kidney disease (CKD) forcefully supports the need for collaboration among nephrologists, cardiologists, diabetologists and general practitioners, to reduce the cardiovascular risk of CKD patients and delay the start of dialysis. Many studies confirm that reducing the dietary intake of proteins improves uremia as well as acid-base and phosphorus disorders without exposing the CKD patient to the risk of malnutrition. The possibility of delaying renal death and the start of dialysis by almost one to two years is also recognized, thanks in part to the antiproteinuric effect of low-protein diets supplemented with keto acids and essential amino acids. Reducing the dietary protein intake delays the start of dialysis independently of the effect of renin-angiotensin system (RAS)-active antihypertensive drugs. Reduction of the dietary protein intake is indicated in patients with a glomerular filtration rate <25 mL/min (CKD stages 4 and 5). Some situations may, however, require an earlier switch to a low-protein diet, e.g., high proteinuria, renal function worsening at more than 5 mL/min/year, diabetes, and metabolic decompensation. If well designed and properly carried out, reduction of the dietary intake of proteins is not associated with low serum albumin levels or malnutrition, and does not affect patients death. Today, highly palatable, high-quality reduced protein preparations are widely available to reduce the protein intake of CKD patients.
 ...
PMID:[Low-protein diet in Italy today: the conclusions of the Working Group from the Italian Society of Nephrology]. 1882 36

Thalassemia is a hereditary anemia resulting from defect in hemoglobin production. Beta thalassemia is due to impaired production of beta globin chains, leading to a relative excess of alpha globin chains. The term beta thalassemia minor is used to describe heterozygotes, who carry one normal beta globin allele and one beta thalassemic allele. The vast majority of these patients are asymptomatic. However, a variety of renal tubular abnormalities including hypercalciuria, hypo-magnesemia with renal magnesium wasting, decreased tubular absorption of phosphorus, hypo-uricemia with renal uric acid wasting, renal glycosuria and tubular proteinuria have been described even in patients with beta thalassemia minor. We here in report a 24-year old female patient who was found to have thalassemia minor and nephrocalcinosis with evidence of renal tubular dysfunction. Investigations revealed normal renal function, hypercalciuria, reduced tubular reabsorption of phosphorus, hypomagnesemia and renal magnesium wasting. Screening for aminoaciduria was found to be negative. An acid loading test revealed normal urinary acidification. Ultrasonogram of the abdomen revealed nephrocalcinosis and splenomegaly. Detailed work up for anemia showed normal white cell and platelet count while peripheral smear showed microcytic hypochromic anemia with few target cells. Hemoglobin electrophoresis revealed hemoglobin A of 92%, hemoglobin A2 of 6.2% and hemo-globin F of 1.8% consistent with beta thalassemia minor. Her parental screening was normal. A diagnosis of beta thalassemia minor with renal tubular dysfunction was made and the patient was started on thiazide diuretics to reduce hypercalciuria and advised regular follow-up.
 ...
PMID:Renal tubular dysfunction with nephrocalcinosis in a patient with beta thalassemia minor. 1897 85


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>