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)

Ovarian hyperstimulation syndrome (OHSS) is a potentially fatal condition associated with the use of ovulation-inducing drugs. We describe a 28-year-old woman who presented with ascites, oliguria and vomiting. Over 2 weeks, the combination of intractable vomiting, intravenous rehydration, paracentesis, hypercatabolism and proteinuria led to severe hypoalbuminaemia with gross oedema and progressively worsening liver function. The patient's albumin dropped to 9 g/l with liver function abnormalities peaking at: alanine aminotransferase, 462 IU/l; alkaline phosphatase, 706 IU/l; bilirubin, 26 micromol/l; and prothrombin time, 19 s. The judicious use of paracentesis and commencement of total parenteral nutrition coincided with a rapid clinical improvement. One month after discharge, the patient was asymptomatic with normal liver function. This case demonstrates the severity of malnutrition and liver dysfunction that can occur with severe OHSS. Increasing use of in-vitro fertilization techniques makes it mandatory for clinicians to be aware of the clinical features, complications and treatment of this condition, and we would suggest that patients with severe OHSS should be jointly managed by physicians and obstetricians.
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PMID:A severe case of ovarian hyperstimulation syndrome with liver dysfunction and malnutrition. 1216 89

A 57-year-old woman was scheduled to receive recombinant interferon-alpha retreatment for chronic active hepatitis C. During the course of therapy, the patient showed rapid onset of oliguria, dizziness, edema, and a pre-shock state. She was subsequently admitted to hospital and was diagnosed as having nephrotic syndrome. After admission, albumin-dominant proteinuria persisted despite the discontinuation of interferon therapy. Light microscopy of a renal needle biopsy specimen showed interstitial lymphoid cell infiltration, but no marked changes of the glomeruli and no staining for immunoglobulin or complement. Electron microscopy showed diffuse effacement of the glomerular epithelial foot processes, leading to a diagnosis of minimal change nephrotic syndrome with interstitial nephritis. Proteinuria resolved after the initiation of oral prednisolone therapy (1 mg/kg per day). The number of patients with chronic hepatitis C requiring interferon retreatment is increasing rapidly. We herein report this rare case of acute onset of nephrotic syndrome during interferon-alpha retreatment.
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PMID:Acute onset of nephrotic syndrome during interferon-alpha retreatment for chronic active hepatitis C. 1242 71

A 66-year-old man with erysipelas was admitted with complaints of oliguria and massive proteinuria/hematuria. He was diagnosed as having acute poststreptococcal glomerulonephritis(APSGN) due to erysipelas infected by group A streptococcus pyogenes. On admission, his white cell count increased to 31,000, and CRP was 27.3 mg/dl. Serum urea nitrogen and creatinine were increased to 90.1 mg/dl and 4.5 mg/dl, respectively. He had diabetes mellitus(HbA1c 7.9%) and liver dysfunction(total bilirubin 3.5 mg/dl, AST 76 IU, ALT 41 IU) caused by alcoholic liver cirrhosis. Hypocomplementemia was found in addition to ASO 216 U/ml and ASK 10,240 x. After antibiotics treatment was initiated, inflammation of the erysipelas began to improve. Disseminated intravascular coagulation syndrome, probably due to sepsis, occurred on the 5th hospital day. He died of gastrointestinal bleeding on the 18th hospital day. Renal autopsy revealed 37% formation of fibrocellular crescents, and marked mesangiolysis was noted by light microscopy. Granular deposition of C3 and IgG was seen along the capillary walls on immunofluorescence study. Intramembranous deposits were scattered on electron microscopy. This case illustrates a fulminant type of APSGN, which was in part attributed to the presence of diabetes and alcoholic liver cirrhosis. Histological findings of crescent formation and marked mesangiolysis may account for the fulminant clinical course.
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PMID:[A case of fulminant acute poststreptococcal glomerulonephritis showing mesangiolysis and crescent formation preceded by erysipelas]. 1247 94

Acute nephritic syndrome is clinically characterized by hematuria, proteinuria, oliguria, and volume overload with or without azotemia and histologically be acute proliferative glomerulonephritis. Acute post streptococcal glomerulonephritis is the commonest cause in children. There is a preceding infection prior to this condition in majority. This is one of the comonest causes of renal edema in children. Early recognition, prompt and aggressive therapy and adequate follow-up are mandatory. Prognosis is usually good unless associated with severe renal failure and crescentic glomerulonephritis where the outcome is relatively poor unless treatment is early and adequate. Pathologically acute proliferative nephritis is with diffuse proliferative glomerulonephritis with or without crescents. Immunosuppressive therapy is not needed in simple acute proliferative glomerulonephritis but is essential in modifying the outcome of crescentic glomerulonephritis. Delayed resolution, severe renal failure at onset, progressive renal failure and associated systemic features like skin rashes, joint pains, hepatosplenomegaly and persistent fever are the indications for biopsy. Overall the prognosis in classical post streptococcal acute proliferative glomerulonephritis is good.
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PMID:Acute and crescentic glomerulonephritis. 1255 62

Denys-Drash syndrome is a rare disorder consisting of pseudohermaphrodism, Wilms' tumor and nephropathy. We describe here a boy with severe hypospadias and undescended testes, who presented with end-stage renal failure at the age of 1 year and 8 months when he was referred to our hospital. Emergency hemodialysis was performed because of oliguria, edema and severe hypertension, and then peritoneal dialysis was started. The findings of the renal biopsy showed diffuse mesangial sclerosis, consistent with the characteristic change in Denys-Drash syndrome. The analysis of WT1 gene revealed a G-to-A point mutation at 1,186 resulting in a change from Asp to Asn at 396 in exon 9. Since he had no urine output and his kidneys were not functional and in addition, patients with this mutation have been reported to have a high risk of Wilms' tumor, bilateral nephrectomy was performed. The removed kidneys showed no malignancies. Since Denys-Drash syndrome is frequently associated with Wilms' tumor, renal biopsy and gene analysis should be performed on male patients with gonadal anomaly, such as hypospadias and/or undescended testes, and proteinuria.
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PMID:[A case of Denys-Drash syndrome with prophylactic bilateral nephrectomy]. 1268 Mar 20

Sonographic findings of renal medullary hyperechogenicity have been observed in the neonate in association with severe perinatal renal injury, kidney malformations or nephrocalcinosis, and, rarely, in newborn infants with transient renal failure. The aim of the study was to describe the entity of neonatal transient renal failure with renal medullary hyperechogenicity (NTRFMH). We studied nine term neonates, born between August 1999 and February 2004 in our institution (0.1% of the live born infants), who developed transient renal dysfunction after birth, and in whom renal sonograms showed bilateral medullary hyperechogenicity. Seven of the infants (78%) had anuria until 30-45 hours of age, and two (22%) had oliguria. Peak serum creatinine levels ranged between 0.61 and 1.62 mg/dL (mean: 1.09+/-0.27 mg/dL) at 2-3 days of life. Additional findings included proteinuria in nine infants (100%), uric acid crystalluria in seven (78%), hyperuricemia in four (44%), and hypertension in one (11%). Hyperuricosuria was demonstrated in one out of the seven patients in whom this parameter was determined. Urinary excretion rates of calcium, phosphorus and oxalic acid were normal, as were urinary levels of amino acids and organic acids. Full clinical recovery accompanied by normalization of all laboratory parameters was observed in all infants by 4-6 days of life. Subsequent follow-up showed normal renal function, no urinary abnormalities, and normal renal sonograms in all infants. Our summary of the nine infants with NTRFMH reported on here and a review of 19 cases of this condition reported in the literature reveal a not-so-rare entity of unclear etiology, but excellent prognosis. Physicians caring for neonates should be aware of this benign and transient condition.
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PMID:Neonatal transient renal failure with renal medullary hyperechogenicity: clinical and laboratory features. 1588 Feb 71

We present a patient from Germany with Hantavirus infection, admitted in the Emergency room of our hospital, with fever, thrombocytopenia, acute renal failure, oliguria, mild proteinuria and hematuria. Percutaneous renal biopsy revealed an acute interstitial nephritis without medulla haemorrhages. The virus infection confirmation was made by detection of IgM against Hantavirus Puumala. This infection should be considered in patients with thrombocytopenia, fever and acute renal failure, over all if they are from North and Central Europe.
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PMID:[Nephropathia caused by hantavirus puumala: a case report]. 1639 14

We describe the case of 24-years old man, smoking up to 60 cigarettes daily, with rapidly progressive crescentic glomerulonephritis in the course of Goodpasture's syndrome. The disease was initially presented with recurrent diffuse pulmonary hemorrhage with normal renal function and moderate proteinuria and haematuria on urinalysis lasting 2 months. Immunologic tests for ANCA and anti-GBM Ab were negative until the patient's renal function rapidly deteriorated during next 3 weeks. At the time of the diagnosis patient presented with renal insufficiency with oliguria requiring hemodialysis but without pulmonary hemorrhage. Renal biopsy showed cellular crescents in all glomeruli with linear deposition of IgG along the GBM. Repeated testing showed anti-GBM Ab. The patient received pulse cyclophosphamide, and pulse methylprednisolone continued by oral prednisone, and consecutive plasma exchange treatment but remained oliguric after 3 weeks of the treatment. The case confirm that in Goodpasture's syndrome even several days' delay in diagnosis and treatment has a strongly negative impact on outcome.
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PMID:[Recurrent alveolar hemorrhage in the course of Goodpasture's syndrome]. 1653 89

Hypertension in pregnancy is one of the main causes of maternal, fetal and newborn morbidity and mortality in civilised countries. Current recommendations of the European Society for Hypertension prefer definition of hypertension in pregnancy based on absolute values of blood pressure, i.e. systolic blood pressure > or = 140 mm Hg or diastolic blood pressure > or = 90 mm Hg. The most important task of classification of hypertension in pregnancy is to distinguish whether hypertension comes before pregnancy (the so called pre-existing hypertension) or whether it is a pregnancy-induced condition (the so called gestational hypertension). Pre-existing hypertension is diagnosed either before pregnancy or within the first 20 weeks of pregnancy. Gestational hypertension is characterised with poor blood circulation in many body organs, higher value of blood pressure usually being just one of the characteristic features. Non-pharmacological treatment of hypertension must be considered in pregnant women with systolic blood pressure 140-150 mm Hg or diastolic blood pressure 90-99 mm Hg. Salt restriction is not recommended, as well as weight reduction in obese women. Systolic blood pressure > or = 170 mm Hg or diastolic blood pressure > or = 110 mm Hg in pregnant women must be considered serious condition necessitating hospitalisation. Pharmacological therapy should include labetalol i.v. or metyldopa or nifedipin administered orally. Intravenous administration of dihydralazine is no longer a therapy of choice, for its use is connected with increased occurrence of adverse effects. The threshold values for commencement of anti-hypertension therapy are systolic blood pressure 140 mm Hg or diastolic blood pressure 90 mm Hg in females with gestational hypertension without proteinuria or with pre-existing hypertension before commencement of 28th week of pregnancy. Drug administration to reduce hypertension is instituted after reaching the same threshold values in females with gestational hypertension and proteinuria or after occurrence of the symptoms any time during pregnancy, with the same threshold values of blood pressure in the case of pre-existing hypertension at the presence of accompanying diseases or organ malfunction and further in the case of pre-existing hypertension and gestational hypertension. In other cases drug treatment of hypertension is recommended at systolic blood pressure values of 150 mm Hg or diastolic blood pressure values of 95 mm Hg. Unless serious hypertension is involved, the drugs of choice include metyldope, labetalol, calcium channel blockers and beta-blockers. Calcium channel blockers are considered safe, unless administered concurrently with magnesium sulphate (risk of hypotension in the case of potential synergism). ACE inhibitors and angiotensine blockers II (AT1-blockers) are contraindicated in pregnancy. Treatment with diuretics is not substantiated, unless oliguria is present. I.v. magnesium sulphate is recommended for prevention of eclampsia and spasm treatment.
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PMID:[Hypertension in pregnancy]. 1672 58

The purpose of this review was to examine the impact of varying degrees of renal insufficiency on pregnancy outcome in women with chronic renal disease. Our search of the literature did not reveal any randomized clinical trials or meta-analyses. The available information is derived from opinion, reviews, retrospective series, and limited observational series. It appears that chronic renal disease in pregnancy is uncommon, occurring in 0.03-0.12% of all pregnancies from two U.S. population-based and registry studies. Maternal complications associated with chronic renal disease include preeclampsia, worsening renal function, preterm delivery, anemia, chronic hypertension, and cesarean delivery. The live birth rate in women with chronic renal disease ranges between 64% and 98% depending on the severity of renal insufficiency and presence of hypertension. Significant proteinuria may be an indicator of underlying renal insufficiency. Management of pregnant women with underlying renal disease should ideally entail a multidisciplinary approach at a tertiary center and include a maternal-fetal medicine specialist and a nephrologist. Such women should receive counseling regarding the pregnancy outcomes in association with maternal chronic renal disease and the effect of pregnancy on renal function, especially within the ensuing 5 years postpartum. These women will require frequent visits and monitoring of renal function during pregnancy. Women whose renal disease is further complicated by hypertension should be counseled regarding the increased risk of adverse outcome and need for blood pressure control. Some antihypertensives, especially angiotensin-converting enzyme inhibitors and angiotensin-receptor blockers, should be avoided during pregnancy, if possible, because of the potential for both teratogenic (hypocalvaria) and fetal effects (renal failure, oliguria, and demise).
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PMID:Chronic renal disease in pregnancy. 1713 89


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