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)

Chronic renal disease with elevated level of serum creatinine (Cr) often progresses to end-stage renal disease. Although blockade of the renin-angiotensin system has been shown to slow the progression of chronic renal disease, it remains uncertain whether one could expect such a renoprotective effect even when the treatment is initiated late in the course of renal disease. The purpose of the present study was to examine the effect of losartan, an angiotensin-II receptor antagonist, on the progression of advanced renal insufficiency. We retrospectively analyzed eight hypertensive patients, whose baseline Cr levels exceeded 2.0 mg/dl (2.2-5.5); the subjects included 6 non-diabetic glomerular diseases, 1 diabetic nephropathy and 1 polycystic kidney disease. Losartan was given at the dosage of 25-50 mg/day. Changes in mean blood pressure (MBP) and serum levels of Cr, potassium (K) and uric acid were evaluated after treatment for 24 weeks. Slopes of reciprocal of serum Cr plotted against time (1/sCr slope), which indicate the rate of renal function loss before and after the treatment period, were compared. There was a significant reduction of 1/sCr slope after losartan (-0.004 +/- 0.002 dl/mg/week before and -0.001 +/- 0.002 dl/mg/week after the treatment, p < 0.05). MBP and serum levels of Cr, K and uric acid were not changed significantly by losartan treatment. However, improvement of 1/sCr slope was correlated to the degree of MBP changes. Based on the available data from 4 patients, proteinuria was decreased in 3 patients. These results suggest that losartan may retard the progression of advanced renal insufficiency.
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PMID:Losartan, an angiotensin-II receptor antagonist, retards the progression of advanced renal insufficiency. 1663 17

Extracellular matrix abnormalities have been found in both human and animal models of polycystic kidney disease (PKD). A new mouse PKD model has been produced through insertion of a PGKneo cassette in an intron of the gene that encodes laminin alpha5 (Lama5), a major tubular and glomerular basement membrane component that is important for glomerulogenesis and ureteric bud branching. Lama5neo represents a hypomorphic allele as a result of aberrant splicing. Lama5neo/neo mice exhibit PKD, proteinuria, and death from renal failure by 4 wk of age. This contrasts with mice that totally lack Lama5, which die in utero with multiple developmental defects. At 2 d of age, Lama5neo/neo mice exhibited mild proteinuria and microscopic cystic transformation. By 2 wk, cysts were grossly apparent in cortex and medulla, involving both nephron and collecting duct segments. Tubular basement membranes seemed to form normally, and early cyst basement membranes showed normal ultrastructure but developed marked thickening as cysts enlarged. Overall, Lama5 protein levels were severely reduced as a result of mRNA frameshift caused by exon skipping. This was accompanied by aberrant accumulation of laminin-332 (alpha3beta3gamma2; formerly called laminin-5) in some cysts, as also observed in human PKD. This constitutes the first evidence that a primary defect in an extracellular matrix component can cause PKD.
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PMID:A hypomorphic mutation in the mouse laminin alpha5 gene causes polycystic kidney disease. 1679 May 9

A 70-year-old man with polycystic kidney disease developed nephrotic syndrome, deteriorating to renal insufficiency. Histological examination revealed IgA nephropathy. With treatment of prednisolone, an angiotensin-converting enzyme inhibitor, and an angiotensin II receptor-blocker, his proteinuria markedly decreased and renal function was stabilized. This case supports the idea that renal biopsy is needed in patients with polycystic kidney disease with nephrotic-range proteinuria, for appropriate treatment and prevention of renal failure.
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PMID:Nephrotic syndrome and IgA nephropathy in polycystic kidney disease. 1679 1

Recently, there has been extensive debate about extending the criteria for accepting living donors to include the presence of mild renal abnormalities such as isolated microhematuria. Hematuria defined as the detection of greater than five red blood cells per high power field can be associated with abnormalities throughout the urinary tract. Detection of casts or dysmorphic red blood cells in the urine sediment with or without proteinuria could indicate underlying intrinsic renal disease. Anatomic causes, such as stones and tumors, should be excluded; cystoscopy may be indicated to exclude bladder pathology. Obviously, urinary tract infection, uncontrolled hypertension and latent diabetes mellitus must be excluded. Microscopic hematuria could be associated with mesangial IgA deposits; as 10% of first-degree relatives of patients with IgA glomerulonephritis suffer from microhematuria and/or proteinuria that may require consideration of renal biopsy. Microhematuria could also be associated with other known hereditary renal diseases such as C3 deposits disease, IgM nephropathy, autosomal dominant polycystic kidney disease, Alport's syndrome or thin basement membrane disease. In conclusion, careful assessment of isolated microhematuria, in the context of living kidney donation, is mandatory as results may reveal occult renal disease that may contraindicate kidney donation.
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PMID:The renal allograft donor with isolated microhematuria. 1697 Feb 50

The use of prenatal ultrasonography has resulted in increased numbers of fetuses being diagnosed with autosomal dominant polycystic kidney disease (ADPKD), but the long-term prognosis is still not well-known. Between 1981 and 2006 we followed 26 consecutive children with enlarged hyperechoic kidneys detected between the 12th week of pregnancy and the first day of life (Day 1) as well as one affected parent. Three other fetuses were excluded following the termination of the pregnancy. The mother was the transmitting parent in 16 of the 26 children (ns, p=0.1). Clinical features that presented during follow-up were oligoamnios (5/26), neonatal pneumothorax (3/26), pyelonephritis (5/26), gross hematuria (2/26), hypertension (5/26), proteinuria (2/26) and chronic renal insufficiency (CRI) (2/26). At the last follow-up (mean duration of follow-up: 76 months; range: 0.5-262 months), 19 children (mean age: 5.5 years) were asymptomatic, five (mean age: 8.5 years) had hypertension, two (mean age: 9.7 years) had proteinuria and two (mean age: 19 years) had CRI. Children presenting enlarged kidneys postnatally tended to have more clinical manifestations than their counterparts who did not. Of 25 siblings of the patients, seven had renal cysts; these were detected during childhood in five siblings and in utero in two siblings. In conclusion, prognosis is favourable in most children with prenatal ADPKD, at least during childhood. The sex of the transmitting parent is not a risk factor of prenatal ADPKD. A high proportion of siblings develop early renal cysts. Abnormalities visualized by ultrasonography appear to be associated to more clinical manifestations.
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PMID:Prognosis of autosomal dominant polycystic kidney disease diagnosed in utero or at birth. 1712 4

Flaxseed derivatives, including both oil and flax lignan, modify progression of renal injury in animal models, including Han:SPRD-cy polycystic kidney disease (PKD). Gender is a significant factor in the rates of progression of many forms of human renal disease, but the role of gender in the response to nutrition intervention in renal disease is unexplored. In this study, male and female Han:SPRD-cy rats or normal littermates were fed either corn oil (CO) or flax oil (FO) diets, with or without 20 mg/kg of the diet flax lignan secoisolaricinoresinol dyglycoside (SDG). Renal injury was assessed morphometrically and biochemically. Renal and hepatic PUFA composition was assessed by GC and renal PGE2 release by ELISA. FO preserved body weight in PKD males, with no effect in females. SDG reduced weight in both normal and PKD females. FO reduced proteinuria in both male and female PKD. FO reduced cystic change and renal inflammation in PKD males but reduced cystic change, fibrosis, renal inflammation, tissue lipid peroxides, and epithelial proliferation in PKD females. SDG reduced renal inflammation in all animals and lipid peroxides in PKD females. A strong interaction between SDG and FO was observed in renal FA composition of female kidneys only, suggesting increased conversion of C18 PUFA to C20 PUFA. FO reduced renal release of PGE2 in both genders. Gender influences the effects of flaxseed derivatives in Han:SPRD-cy rats. Gender-based responses to environmental factors, such as dietary lipid sources and micronutrients, may contribute to gender-based differences in disease progression rates.
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PMID:Effects of flaxseed derivatives in experimental polycystic kidney disease vary with animal gender. 1726 60

Autosomal-dominant polycystic kidney disease is an inherited disorder characterized by the development and growth of cysts in the kidneys. Urinary protein excretion is generally less than 1 g/day, and the association of the nephrotic syndrome with this condition is considered rare. A 39-year-old man with autosomal-dominant polycystic kidney disease and nephrotic-range proteiuria is described. During admission, he had general edema and a diagnosis of pulmonary tuberculosis. The patient had hyperlipidemia, hypoalbuminemia, and 11.8 g/day proteinuria. The gingiva and rectum biopsies were performed in order to evaluate the etiology of nephrotic syndrome, and revealed AA amyloidosis thought to be secondary to pulmonary tuberculosis. We maintained the antituberculous treatment and began colchicine at a dose of 2 g/day and candesartan 8 mg/day. To our knowledge, this is the first autosomal-dominant polycystic kidney disease case with nephrotic syndrome due to amyloidosis secondary to pulmonary tuberculosis.
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PMID:Amyloidosis in a patient with autosomal dominant polycystic kidney disease and tuberculosis: a case report. 1731 53

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.
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PMID:Glomerular polycystic kidney disease in a dog (blue merle collie). 1742 9

Diagnosis and treatment of autosomal dominant polycystic kidney disease (ADPKD) is rapidly changing. Cellular pathways that involve the polycystins are being mapped and involve the primary cilium, intracellular calcium and cAMP regulation, and the mammalian target of rapamycin (mTOR) pathway. With the use of new imaging approaches, earlier diagnosis of hepatic cystic disease is possible, and measurement of kidney and cystic growth as well as kidney blood flow is possible over relatively short periods. PKD gene type, gender, proteinuria, and the presence of hypertension relate to the rate of kidney growth in ADPKD. On the basis of risk factors for progression to ESRD and the pathogenic roles that intracellular cAMP and mTOR play in cystogenesis, novel therapies are now being tested, including maximal inhibition of the renin-angiotensin system, inhibition of renal intracellular cAMP using vasopressin V2 receptor antagonists, and somatostatin analogues, as well as inhibitors of mTOR. This review addresses the current understanding of the pathogenesis and the natural history of ADPKD; accuracy and reliability of diagnostic approaches in utero, childhood, and adulthood; the value of reliable magnetic resonance imaging to measure disease progression early in the course of ADPKD; and novel therapeutic approaches that are being evaluated in ADPKD.
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PMID:Autosomal dominant polycystic kidney disease: time for a change? 1742 47

For determination of the incidence of renal events in autosomal dominant polycystic kidney disease (ADPKD) all patients who had ADPKD and attended nephrology/urology clinics in Newfoundland in 1981 were identified, and members of 18 families who were at 50% risk for inheriting ADPKD were followed prospectively for 22 yr, including research clinics at 6-yr intervals. Time to hypertension treatment, stage 3 chronic kidney disease (CKD), ESRD, and death was measured, and the impact of genotype, gender, gender of parent who transmitted PKD, family, family history of essential hypertension, parity, and oral contraceptive pill was assessed. Nine (50%) families had PKD1, four (22%) had PKD2, and one had both PKD1 and PKD2. The number of family members with PKD1 was 136 and with PKD2 was 60. In PKD1 median age to hypertension treatment was 46 yr, to CKD stage 3 was 50 yr, to ESRD was 53 yr, and to death was 67 yr. In PKD2, median age to hypertension treatment was 51 yr, to CKD stage 3 was 66 yr, to death was 71 yr, and ESRD was infrequent. Although the incidence of CKD was later and ESRD occurred infrequently in PKD2 compared with PKD1, early onset of hypertension occurred and life expectancy was compromised. Genotype, family, and proteinuria were identified as risk factors for incident renal events. Gender, gender of parent who transmitted PKD, family history of essential hypertension, multiparity, and use of the oral contraceptive pill were not identified as risk factors for renal events in ADPKD.
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PMID:Incident renal events and risk factors in autosomal dominant polycystic kidney disease: a population and family-based cohort followed for 22 years. 1769 77


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