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

Hyponatremic hypertensive syndrome is a manifestation of severe hypertension related to renal ischemia. The most common underlying cause of hyponatremic hypertensive syndrome in adults is severe atherosclerotic reno-vascular disorder while in children the most common cause of hyponatremic hypertensive syndrome is unilateral congenital renal artery stenosis due to some form of arterial dysplasia. An excessively stimulated renin-angiotensin-aldosterone system is mainly responsible for heavy polyuria, renal electrolyte loss and proteinuria. The neurological manifestations of hyponatremia and/or hypertensive encephalopathy are the main presenting symptoms, and they are not always in linear correlation with the degree of hyponatremia and/or hypertension. The cornerstone of management is the treatment of underlying hypertensive disease, but the correction of hyponatremic dehydration and safe decrease of blood pressure are essential in the emergency phase of hyponatremic hypertensive syndrome. The optimal antihypertensive therapy depends on the underlying condition. Revascularization, either surgical or by percutaneous transluminal angioplasty, is recommended for children with renal artery stenosis. Pharmacological treatment based on ACEI and/or ARB is the most efficient antihypertensive therapy for those with ischemic reno-parenchymal disorder. Nephrectomy is required if an affected kidney contributes less than 10% of the global renal function, if percutaneous transluminal angioplasty fails and the operative risk is too high, or in the case of extensive tumorous lesions.
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PMID:Hyponatremic hypertensive syndrome. 1892 57

Renal venous thrombosis (RVT) is a rare but a well recognized entity in children and neonates. The clinical signs of neonatal RVT include hypertension, enlarged kidney(s), hematuria, renal insufficiency, proteinuria, thrombocytopenia, or all. Persisting impairment of kidney function and hypertension are serious and common complications in patients with RVT. Risk factors for the development of RVT include maternal diabetes mellitus, pathologic states associated with thrombosis (e.g., shock, dehydration, perinatal asphyxia, polycythemia), and sepsis. Inherited prothrombotic abnormalities have been described in some reports of RVT. We report the case of a male newborn with left RVT and associated homozygosity for both factor V Leiden (G1691A) and methylenetetrahydrofolate reductase C677T mutations in addition to elevated serum lipoprotein (a). The patient was treated with heparin. We believe our case to be the first reported case in the English medical literature of such an association between neonatal RVT and homozygosity for both factor V Leiden and methylenetetrahydrofolate reductase. This case and other studies clearly demonstrate that neonatal RVT should be evaluated for thrombophilia conditions.
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PMID:Renal venous thrombosis in a newborn with prothrombotic risk factors. 1954 80

Strongyloidiasis, a chronic infection caused by the intestinal parasite Strongyloides stercoralis, is prevalent in the Nansei Islands of Japan. Here, we report our findings on a case of strongyloidiasis complicated with steroid-resistant minimal change nephrotic syndrome in a 69-year-old male resident of Fukuoka Prefecture who had lived in Yakushima, one of the Nansei Islands, until age 15. In October 2006, he developed proteinuria and edema, and was diagnosed with minimal change nephrotic syndrome on the basis of the renal biopsy findings. Following treatment with prednisolone, the level of proteinuria decreased to 0.29 g/day by day 35. However, 5 days later (day 40), the patient developed persistent watery diarrhea and vomiting, leading to dehydration and malnutrition. Pneumonia and bacterial meningitis subsequently developed (day 146); filarial (infectious-type) and rhabditiform (noninfectious-type) S. stercoralis larvae were detected for the first time in the patient's sputum, gastric juice, feces, and urine. Although treatment with ivermectin was started immediately and the parasitosis responded to the treatment, the patient died of sepsis. Consequently, although strongyloidiasis is a rare infection except in endemic regions, it is essential to consider the possibility of this disease and begin treatment early for patients who have lived in endemic areas and who complain of unexplained diarrhea during steroid-induced or other immunosuppression.
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PMID:Minimal change nephrotic syndrome in a patient with strongyloidiasis. 2146 22

In January 2003, a 70-year-old female consulted a doctor for a fever of unknown origin. She had microscopic hematuria, proteinuria, BUN 41 mg/dL, Cr 2.1 mg/dL and MPO-ANCA 44 U/mL, and was suspected of having ANCA-associated nephritis. A renal biopsy was not conducted because the patient had just one kidney. She was treated with prednisolone (PSL ; 40 mg/day). Subsequently, because of Cr level improvement, the amount of PSL was decreased. In October 2006, the patient again had microscopic hematuria, proteinuria and a slightly elevated Cr level. Lowering of BP and dehydration caused by a common cold were considered to be the cause of her renal dysfunction. She was admitted to Fukuoka University Hospital for 2 weeks, where she received diet therapy and a changed medication schedule in which furosemide was stopped and the dose of enalapril was decreased from 5 mg/day to 2.5 mg/day. Because the MPO-ANCA level was < 10 EU, the amount of PSL was not changed. After 11 months, treatment with lansoprazole at 30 mg/day was started. At the end of the same month, however, she exhibited gait disturbance due to swelling, redness and tenderness in the bilateral pedal joints. After one month of receiving lansoprazole, she experienced a high fever and an elevated Cr level. Accordingly she was again admitted to the hospital, where she was diagnosed with venous thrombosis in the lower limbs, and warfarization was begun. Her condition improved, gradually, and she was discharged from the hospital. After the discharge, she began to exhibit watery diarrhea three to four times per day. Therefore, treatment with warfarin potassium was stopped 50 days after it was begun. In spite of the cessation of warfarization, the diarrhea continued. She underwent bacterial culturing and lower endoscopic examinations (no biopsy was done), which showed erosion of the colon, but the cause of the diarrhea was not found. After 181 days of treatment with lansoprazole, administration of this drug was stopped. The symptoms disappeared within 5 days. There have been few reports of collagenous colitis with chronic diarrhea, but a good prognosis has been described in these cases. Clinicians should consider drug treatment as a possible cause of collagenous colitis in the case of patients with chronic diarrhea of unknown origin during the administration of medication.
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PMID:[Case of suspicious lansoprazole-associated collagenous colitis in ANCA-associated nephritis]. 2041 35

Serum electrolytes and urine analysis results were retrospectively reviewed in children with either dengue fever (DF) or dengue hemorrhagic fever (DHF). Children who had positive serology for dengue infection and serum electrolytes determined before starting intravenous fluid were included in the study. During the years 2004-2007, 73 DF patients, age 9.29 +/- 3.62 years, and 77 DHF patients, age 10.04 +/- 3.64 years were enrolled in the study. The patients were admitted to the hospital on average on days 4.12 +/- 1.1 and 4.25 +/- 1.4 of febrile illness for DF and DHF, respectively. The prevalence of hyponatremia in patients with DF was 61% and DHF was 72% (p = 0.149). The mean serum sodium levels in patients with DF and DHF were 133.5 +/- 3.52 and 133.5 +/- 3.20 mEq/l (p = 0.938), respectively. The prevalence of hyponatremia in patients with mild (grade I), moderate (grade II) and severe (grade III-IV) DHF were 70, 77, and 78% (p = 0.729), respectively, and the mean serum sodium levels were 134.1 +/- 3.05, 132.9 +/- 3.33, and 132.5 +/- 3.28 (p = 0.189), respectively. The prevalence of hypokalemia in patients with DF was 14% and 17% in patients with DHF (p = 0.588). A high urine specific gravity reflecting dehydration was found in 63% of patients with DF and 60% of patients with DHF (p = 0.77). The prevalences of hematuria in patients with DF and DHF were 18% and 27% (p = 0.182), respectively and proteinuria were 15% and 27% (p = 0.072), respectively. The prevalences of hematuria and proteinuria were not different among patients with mild, moderate and severe DHF. No patients had gross hematuria or developed acute renal failure requiring dialysis. Mild hyponatremia is a common electrolyte disturbance and renal involvement is mild in patients with DF and DHF.
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PMID:Electrolyte disturbances and abnormal urine analysis in children with dengue infection. 2057 84

This review explores the current model of sickle cell nephropathy and the limitations of the model. Renal abnormalities are common complications of sickle cell disease (SCD). Beginning in childhood, patients with SCD develop a urinary concentrating defect resulting in polyuria and a predisposition to nocturnal enuresis and dehydration. The current model of sickle cell nephropathy suggests that destruction of the renal medulla induces production of renal vasodilating substances that feedback to the glomerulus causing hyperfiltration. Hyperfiltration leads to glomerulosclerosis and proteinuria, with eventual reduction in kidney function. The crucial steps of vasodilating substance production and hyperfiltration in children with SCD have not been proven. Treatment of sickle cell nephropathy is aimed at the reduction of proteinuria with angiotensin converting enzyme inhibitors or angiotensin receptor blockers. Hydroxyurea and chronic transfusion therapy may also alter the progression of sickle cell nephropathy in children. Further studies are needed to identify an accurate model and effective treatments for sickle cell nephropathy.
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PMID:Sickle cell nephropathy: challenging the conventional wisdom. 2120 78

A five-year-old boy was referred to our pediatric clinic for evaluation of failure to thrive, headache, intermittent high fever, restlessness, polyuria, and polydipsia. His weight and height measurements were under the 3rd percentile. Clinical findings consisted of frontal bossing, carious teeth, O-bain deformity of the lower extremities, and moderate dehydration. The presence of metabolic alkalosis, hypokalemia, hypochloremia, and high renin and aldosterone levels were suggestive of Bartter syndrome and a treatment regimen for Bartter syndrome was started. At follow-up, the polyuria and hyponatremia were found to persist. A reassessment of the patient revealed findings consistent with proximal renal tubular acidosis such as metabolic acidosis with a high urinary pH, proteinuria, aminoaciduria with phosphaturia and hypercalciuria. Based on the presence of parental consanguinity as well as polyuria, proteinuria, low tubular reabsorption of phosphorus, generalized aminoaciduria, light yellow skin and hair color, the probable diagnosis of cystinosis was established and was confirmed by slit-lamp examination of the cornea showing cystine crystal deposition. Our case is a good example demonstrating that development of metabolic alkalosis does not exclude cystinosis and that all findings of the patient should be thoroughly evaluated.
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PMID:Cystinosis presenting with findings of Bartter syndrome. 2175 Jun 41

Neuroblastoma is the most common extracranial solid tumor in childhood. Its presenting signs and symptoms may be highly variable, depending on the location of the primary tumor and its local or metastatic diffusion and, rarely, with paraneoplastic syndrome such as opsoclonus-myoclonus-ataxia syndrome and gastrointestinal disturbances, due to autoantibodies or to aberrant secretion of vasoactive intestinal peptide. Herein we describe a 10-month-old child with neuroblastoma presenting with a complex clinical picture characterized by acute kidney injury manifested by renal insufficiency and signs and symptoms of tubulointerstitial damage, with polyuria, polydipsia, glucosuria, aminoaciduria and hypochloremic metabolic alkalosis, and of glomerular damage with heavy proteinuria. Imaging study documented a suprarenal mass enveloping the aorta and its abdominal and renal ramifications and bilaterally renal veins. This clinical picture shows some analogies with the hyponatremic-hypertensive syndrome concerning the renovascular disease; however, in absence of systemic arterial hypertension, the heavy proteinuria and the polyuria could be explained by sectional increased intraglomerular pressure, due to local renal blood vessels constriction. Hypochloremic metabolic alkalosis probably developed because of local production of renin, responsible of renin-angiotensin-aldosterone system activation, but above all because of chloride loss through sweating. The long lasting dehydration, due to vomiting, sweating and polyuria, caused prolonged prerenal failure evolving in proximal tubular damage manifestations.
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PMID:Neuroblastoma presenting with acute kidney injury, hyponatremic-hypertensive-like syndrome and nephrotic proteinuria in a 10-month-old child. 2194 89

Fanconi's syndrome is a complex of multiple tubular dysfunctions of proximal tubular cells occurring alone or in association with a variety of inherited (primary) or acquired (secondary) disorders. It is characterized by aminoaciduria, normoglycaemic glycosuria, tubular proteinuria without hematuria, metabolic acidosis without anion gap and excessive urinary excretion of phosphorous, calcium, uric acid, bicarbonate, sodium, potassium, and magnesium. Whereas diabetes insipidus is a disease of collecting tubules and child mainly presents with dehydration and hypernatremia. Though all the cases published till date were secondary to drugs, myeloma, hematological disorders, etc., we are reporting the first case of idiopathic Fanconi's syndrome along with nephrogenic diabetes insipidus in a child who presented to us as resistant rickets. Medline search did not reveal any case of nephrogenic diabetes insipidus associated with idiopathic Fanconi syndrome. We hypothesized that the NDI may be due to of severe hypokalemia induced tubular dysfunction.
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PMID:Nephrogenic diabetes insipidus with idiopathic Fanconi's syndrome in a child who presented as vitamin D resistant rickets. 2202 6

Fanconi's syndrome is a complex of multiple tubular dysfunctions of proximal tubular cells occurring alone or in association with a variety of inherited (primary) or acquired (secondary) disorders. It is characterized by aminoaciduria, normoglycemic glycosuria, tubular proteinuria without hematuria, metabolic acidosis without anion gap and excessive urinary excretion of phosphorous, calcium, uric acid, bicarbonate, sodium, potassium and magnesium. Diabetes insipidus is a disease of collecting tubules and a child mainly presents with dehydration and hypernatremia. We report the first case of idiopathic Fanconi's syndrome along with nephrogenic diabetes insipidus (NDI) in a child who presented to us as resistant rickets. Medline search did not reveal any case of nephrogenic diabetes insipidus associated with idiopathic Fanconi's syndrome. We hypothesized that the NDI may be due to severe hypokalemia induced tubular dysfunction. The child was treated for hypophosphatemic rickets with severe metabolic acidosis and the treatment for NDI was also given. Now he has healed rickets and normal blood pH, sodium and osmolarity.
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PMID:Idiopathic Fanconi's syndrome with nephrogenic diabetes insipidus in a child who presented as vitamin D resistant rickets--a case report and review of literature. 2214 69


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