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

Angiotensin-converting enzyme (ACE) I/D polymorphism has been implicated as a genetic marker for progression of glomerular disease. Studies of ACE genotypes in adults with IgA nephropathy (IgAN) have yielded conflicting results. We performed ACE genotyping on 79 patients with IgAN diagnosed prior to age 18 years who had either progressed to end-stage renal disease (ESRD) or are now more than 5 years post biopsy. Mean follow-up was 14.8 years for those with normal renal function. Forty-three (54.4%) subjects had normal renal function and a normal urinalysis at last evaluation. Sixteen (20%) progressed to ESRD and 1 has chronic renal insufficiency. Kaplan-Meier survival curves for progression to ESRD did not differ significantly for the ACE DD, ID, and II genotype groups (P=0.095, log-rank test). By univariate analysis, presence of hypertension and degree of proteinuria at diagnosis, and unfavorable histology but not ACE genotype, was significantly associated with progression to ESRD. In the Cox proportional hazards model that included grade of proteinuria, the ACE D allele was a significant independent predictor of outcome with a hazard ratio of 2.37 (P=0.031). Our data, while inconclusive, suggest that the ACE D allele may associate with poor outcome in pediatric IgAN.
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PMID:Angiotensin-converting enzyme genotype and outcome in pediatric IgA nephropathy. 1217 61

Sirolimus, being nonnephrotoxic, is a viable alternative in patients who develop renal insufficiency caused by calcineurin inhibitors (CIs). The aim of this study is to determine whether there is improvement in renal function in liver transplant recipients after switching to sirolimus-based immunosuppression. In this retrospective review, patients who were more than 3 years posttransplantation were selected. Patients who had proteinuria (protein > 300 mg/24 hr), those administered any other nephrotoxic agents, and those with a creatinine clearance (CCr) less than 20 mL/min were excluded. Renal insufficiency was defined as mild (CCr > 70 mL/min), moderate (CCr, 40 to 70 mL/min), or severe (CCr, 20 to 40 mL/min). In the 16 patients studied; there was significant improvement in serum blood urea nitrogen (36 mg/dL; range, 19 to 53 mg/dL; to 25 mg/dL; range, 10 to 37 mg/dL; P =.002) and serum creatinine levels (median, 1.95 mg/dL; range, 1.3 to 2.8 mg/dL; to 1.5 mg/dL; range, 1.0 to 2.4 mg/dL; P =.001) 6 months after switching to sirolimus therapy. There also was a trend in improvement in CCr from 43 mL min (range, 24 to 68 mL/min) to 49 mL/min (range, 22 to 152 mL/min). Among 9 patients with moderate renal insufficiency, 2 patients improved to mild renal insufficiency, 4 patients remained unchanged, and 3 patients deteriorated to severe renal insufficiency. Among 7 patients with severe renal insufficiency, 1 patient improved to mild renal insufficiency, 4 patients improved to moderate renal insufficiency, and 2 patients remained unchanged. No patient developed cellular rejection or other graft-related complications. In liver transplant recipients with chronic renal insufficiency, conversion to sirolimus-based immunosuppression allows complete withdrawal of CIs, leading to some improvement in renal function.
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PMID:Sirolimus monotherapy in nephrotoxicity due to calcineurin inhibitors in liver transplant recipients. 1254 5

Podocin is an integral membrane protein encoded by NPHS2, which is mapped to 1q25-31 and is exclusively expressed in glomerular podocytes. NPHS2 mutations are responsible for autosomal recessive familial steroid-resistant nephrotic syndrome (SRNS) with minor glomerular abnormalities or focal segmental glomerulosclerosis (FSGS), which is characterized by early childhood onset (age less than 6 years) and rapid progression to chronic renal insufficiency. This gene mutation is also responsible for an adolescent/adult onset form of autosomal recessive familial FSGS with heavy proteinuria. It has been demonstrated that sporadic SRNS and heavy proteinuria are also due to NPHS2 gene mutations. We isolated genomic DNA from 36 Japanese children with chronic renal insufficiency caused by SRNS or heavy proteinuria, and analyzed all eight exons and exon-intron boundaries of NPHS2 using the polymerase chain reaction and direct sequencing. The age at onset of disease was 3.9+/-0.5 years. There were 29 patients with SRNS and 7 with heavy proteinuria without nephrotic syndrome at the onset, but all patients developed chronic renal insufficiency 4.6+/-0.8 years after the onset. A new homozygous missense variant of NPHS2, G34E (G101A) in exon 1, was detected in 1 of 36 patients. However, this homozygous variant was also found in 1 of 44 normal controls, suggesting that the mutation is a polymorphism. Two silent variants (T954C and A1038G) in exon 8 of this gene were also identified in some of the patients and normal controls, indicating that the silent variants are also polymorphisms. There was no significant difference in the genotypic and allelic frequencies of T954C and A1038G polymorphisms between the patients and normal controls. In conclusion, NPHS2 gene mutations are not a major cause of chronic renal insufficiency caused by sporadic SRNS or heavy proteinuria in Japanese children.
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PMID:NPHS2 mutations in sporadic steroid-resistant nephrotic syndrome in Japanese children. 1268 58

The purpose of this study was to identify clinical, nutritional, and laboratory factors associated with the rate of progression of chronic renal insufficiency among children and adolescents admitted to a pre-end-stage renal failure (ESRF) interdisciplinary program. Sixty-two children and adolescents aged 2 months to 19 years with chronic renal failure on conservative management were prospectively followed from 1990 to 1999. The following variables were analyzed: age at admission, sex, race, blood pressure, primary renal disease, Z scores for weight and height, glomerular filtration rate (GFR), urea, and presence and degree of proteinuria. Progression to ESRF was assigned as a dependent variable. The analysis was conducted in two steps. In a univariate analysis, variables associated with ESRF outcome were identified by the log-rank test. Then, the variables that were significantly associated with adverse outcome were included in a multivariate analysis. This analysis, using the Cox proportional hazards model, was performed to identify variables that were independently associated with a worse prognosis. Only variables that remained independently associated with adverse outcome were included in the final model. Twenty-one (34%) patients evolved to ESRF during a median follow-up of 43 months. Two variables were identified as independent predictors of progression to ESRF: GFR under 30 ml/min (RR=3, 95% CI=1.7-5.3, P=0.0001) and severe proteinuria (RR=3.1, 95% CI=1.2-7.6, P=0.01). The combination of two factors-GFR lower than 30 ml/min and presence of severe proteinuria on admission-was an independent indicator of adverse outcome in children and adolescents with chronic renal insufficiency who were conservatively managed.
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PMID:Predictive factors of progression of chronic renal insufficiency: a multivariate analysis. 1270 Sep 65

Limited data suggest that HMG-CoA reductase inhibitors (statins) may slow loss of renal function in individuals with chronic renal insufficiency. This study was conducted to determine whether pravastatin reduced rates of loss of renal function in people with moderate chronic renal insufficiency. This was a post hoc subgroup analysis of a randomized double-blind placebo controlled trial. Data were analyzed from the CARE study (a randomized trial of pravastatin versus placebo in 4159 participants with previous myocardial infarction and total plasma cholesterol < 240 mg/dl). Participants with estimated GFR (MDRD-GFR) < 60 ml/min per 1.73 m(2) body surface area at baseline were considered to have moderate chronic renal insufficiency. Multivariate regression was used to calculate rates of decline in MDRD-GFR for individuals receiving pravastatin and placebo, controlling for prospectively determined covariates that might influence rates of renal function loss. Change in renal function could be calculated in 3384 individuals, of whom 690 (20.4%) had MDRD-GFR < 60 ml/min per 1.73 m(2) and were eligible for inclusion. Among all individuals with MDRD-GFR < 60 ml/min per 1.73 m(2)), the MDRD-GFR decline in the pravastatin group was not significantly different from that in the placebo group (0.1 ml/min per 1.73 m(2)/yr slower; 95% CI, -0.2 to 0.4; P = 0.49). However, there was a significant stepwise inverse relation between MDRD-GFR before treatment and slowing of renal function loss with pravastatin use, with more benefit in those with lower MDRD-GFR at baseline (P = 0.04). Rate of change in MDRD-GFR in the pravastatin group was 0.6 ml/min per 1.73 m(2)/yr slower than placebo (95% CI, -0.1 to 1.2; P = 0.07) in those with MDRD-GFR < 50 ml/min, and 2.5 ml/min per 1.73 m(2)/yr slower (95% CI, 1.4 to 3.6 slower; P = 0.0001) in those with MDRD-GFR < 40 ml/min per 1.73 m(2)/yr. Pravastatin also reduced rates of renal loss to a greater extent in participants with than without proteinuria at baseline (P = 0.006). It is concluded that pravastatin may slow renal function loss in individuals with moderate to severe kidney disease, especially those with proteinuria. These findings require confirmation by a large randomized trial conducted specifically in people with chronic renal insufficiency.
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PMID:Effect of pravastatin on loss of renal function in people with moderate chronic renal insufficiency and cardiovascular disease. 1276 Dec 62

The commonest clinical presentation of both immunoalergic interstitial nephritis (IIN) and atheroembolic renal disease (ATD) is an acute renal failure accompanied by skin lesions and eosinophilia. As a consequence, differential diagnosis between both entities is often very difficult. We have performed a comparative retrospective study of those patients diagnosed as having IIN or ATD in our Hospital in the period 1980-2000. A total of 42 patients have been diagnosed of IIN and 16 of ATD. Demographic data, as well as clinical and laboratory parameters and outcomes of every studied patient were analysed. We found a significantly higher prevalence of male sex (100% vs 57%, p < 0.01), previous history of hypertension (100% vs 55%, p < 0.01), chronic renal insufficiency (56% vs 17%, p < 0.01), ischemic heart disease (56% vs 14%, p < 0.001), peripheral ischemic disease, endovascular procedures (87% vs 7%, p < 0.001) and anticoagulant treatments (25% vs 5%, p < 0.001) among patients with ATD as compared with IIN, respectively. On the contrary, previous infections (45% vs 12%, p < 0.01) and exposure to new drugs (100% vs 40%, p < 0.001) were significantly more frequent among IIN patients in compare with ATD. ATD patients showed skin lesions consisting of livedo reticularis and digital infarcts (63% vs 31%, p < 0.05) accompanied by blood pressure increase (100% vs 24%, p < 0.001), whereas IIN patients showed fever (41% vs 19%, p < 0.05) and cutaneous rash as significant clinical manifestations, respectively. The number of ATD patients with proteinuria > 1 g/24 h was significantly higher, but no differences between both groups in the prevalence of urinary sediment abnormalities were observed. The prevalence of absolute eosinophilia was high in both groups (88% among ATD patients, 64% among IIN patients; pNS). Prognosis of both entities was clearly different: Almost all patients with ATD died (69%) or evolved to end-stage renal failure, whereas most patients with IIN showed a recovery of renal function after withdrawal of responsible drugs and steroid treatment. In summary, the analysis of clinical and laboratory data allows an initial differential diagnosis in patients suspected as having IIN or ATD.
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PMID:[Immunoallergic interstitial nephritis vs. cholesterol atheroembolism. Differentiating characteristics]. 1277 76

Chronic glomerulonephritis (GN) is one of the leading causes of end-stage renal disease (ESRD). The possibilities for successful treatment in the earliest stages are still limited. Immunosuppressive treatment leads to complete or partial remission only in some patients. Even then, a non-immunological evolution to chronic renal insufficiency often enters a progressive course. By applying a consistent strategy for their individual evaluation and management, it is possible to improve the outcome of patients with GN. The early referral to a nephrologist and an early histomorphological diagnosis; the precise assessment of the type of injury, i.e. proliferative or non-proliferative; the indices of activity and chronicity; and the prognostic indicators are helpful for the therapeutic approach. The goal of the management of GN has to be to suppress the disease with minimum side effects of the treatment. Many unanswered questions and controversies remain concerning the immunosuppressive therapy. A precise distinction is needed between the problematic assertions and evidence-based protocols. A common task for the treatment of all types of chronic GN should be the protection of renal structure and function: control of blood pressure, action on renal haemodynamics and proteinuria via pharmacological inhibition of the renin-angiotensin system, control of hyperlipidaemia and limitation of fibrosis. Some novel and promising pharmacological approaches to extracellular matrix accumulation and chronic interstitial fibrosis are in progress.
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PMID:The treatment of glomerular disease--a compromise between the standard and the individual approach. 1281 65

Metabolic and nutritional care implies procedures which involve normalization or improvement of metabolic deviations in chronic renal insufficiency and failure by dietary and medicamentous means. The therapeutic procedure not only improves some metabolic disorders associated with a decline of the excretory and metabolic endocrinological renal function but can have a positive impact also on progression of renal insufficiency. Conservative treatment thus involves low protein diets, modification of electrolyte and water intake, adjustment of the acid-base balance, Ca, P metabolism, haemogram, hypertension, proteinuria and hyperlipidaemia. In non-diabetic subjects it is sufficient to achieve a glomerular filtration of 0.2 ml/sec. and serum creatinine of 500-600 mumol/l.
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PMID:[Metabolic and nutrition care in patients with chronic renal insufficiency and chronic kidney failure]. 1290 71

The peroxisome proliferator-activated receptor gamma2 (PPARgamma2) Pro12Ala polymorphism has been associated with a decreased risk of type 2 diabetes and a lower albumin excretion rate (AER) in patients with established diabetes. We performed a case-control study aiming to evaluate the association between the Pro12Ala polymorphism and diabetic nephropathy. Genomic DNA was obtained from 104 type 2 diabetic patients (case subjects) with chronic renal insufficiency (78 on dialysis and 26 with proteinuria [AER >or=200 microg/min] and serum creatinine >or=2.0 mg/dl) and 212 normoalbuminuric patients (AER <20 microg/min) with known diabetes duration >or=10 years (control subjects). The genotypic distribution of the PPARgamma2 Pro12Ala polymorphism in these diabetic patients was in Hardy-Weinberg equilibrium, and the Ala allele frequency was 9%. The frequency of Ala carriers (Ala/Ala or Ala/Pro) was 20.3% in control subjects and 10.6% in case subjects (P = 0.031). The odds ratio of having diabetic nephropathy for Ala carriers was 0.465 (95% CI 0.229-0.945; P = 0.034). Carriers of the Ala allele were not different from noncarriers (Pro/Pro) regarding sex (38.9 vs. 44.1% males) or ethnicity (77.4 vs. 71.7% white) distribution, age (61 +/- 10 vs. 61 +/- 10 years), known diabetes duration (17 +/- 7 vs. 16 +/- 7 years), BMI (27 +/- 4 vs. 28 +/- 5 kg/m(2)), fasting plasma glucose (184 +/- 81 vs. 176 +/- 72 mg/dl), HbA(1c) (6.7 +/- 2.3 vs. 6.9 +/- 2.4%; high-performance liquid chromatography reference range: 2.7-4.3%), and systolic (145 +/- 27 vs. 0.144 +/- 24 mmHg) or diastolic (87 +/- 14 vs. 85 +/- 14 mmHg) blood pressure, respectively. In conclusion, the presence of the Ala allele may confer protection from diabetic nephropathy in patients with type 2 diabetes.
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PMID:The human peroxisome proliferator-activated receptor gamma2 (PPARgamma2) Pro12Ala polymorphism is associated with decreased risk of diabetic nephropathy in patients with type 2 diabetes. 1463 65

Early optimalization of the treatment of patients with chronic renal insufficiency can reduce morbidity and deaths. For each patient with a raised serum creatinine concentration, the creatinine clearance should be measured or calculated. When this is abnormal, the cause thereof should be investigated. Chronic renal insufficiency is often progressive, even when the initiating factors are no longer present. Progression can be delayed by treating the high blood pressure, proteinuria and hyperlipidemia by means of a restricted protein diet and advice not to smoke. Acute deterioration of an existing chronic renal dysfunction through dehydration and underfill or through the use of certain medications or toxic substances such as radio-opaque media should be avoided. In patients with chronic renal insufficiency specific attention should be paid not only to hypertension, lipid disturbances, smoking and weight, but also to the calcium-phosphate balance, anaemia and homocysteine levels. The blood pressure, oedema and weight of patients with a clearance between 30-59 ml/min should be checked 2-3 times a year, in addition to laboratory tests for Hb, Ht, creatinine, urea, potassium, calcium, phosphate, pH, bicarbonate and lipid spectrum. It is recommended that when creatinine clearance (< 50 ml/min) falls a nephrologist should be consulted at least once with respect to the strategy to be followed. Symptoms of chronic renal insufficiency can occur when the creatinine clearance is < 30 ml/min. This relates to: sodium retention, imbalances in the calcium and phosphate levels, anaemia, uraemia, water retention, potassium retention and metabolic acidosis. Referral should take place at a creatinine clearance of < or = 30 ml/min.
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PMID:[Treatment of patients with chronic renal insufficiency; a guideline for internists]. 1511 99


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