Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hematuria is the presence of more than 5 RBC's in repeated urinary sediments. Erythrocyturia may be present as an isolated finding or it may be associated to other clinical findings that may lead to the etiology of the hematuria. Its origin may be renal or extrarenal. In the neonate, meatal or urethral bleeding, polycystic kidney or hydronephrosis must be considered. In the infant, hematuria may be due to vascular disease, renal vein thrombosis, as well as to urinary tract infection, urinary tract obstruction or acute tubular interstitial nephritis due to drug ingestion. Primary and secondary glomerulopathies, urinary tract infection and urolithiasis are the most frequent causes of hematuria in pre-school or school-age children. The diagnostic approach emphasizes the importance of the clinical history, familial background and the circumstances of presentation. RBC casts and proteinuria may suggest the presence of a glomerulopathy. Leukocyturia is more frequent in urinary tract infections and requires urine cultures and intravenous pyelogram. In cases of isolated hematuria, blood clotting test, P. T., P.T.T., platelet count and RBC's morphology may be required to rule out hematological disorders. The intravenous pyelogram, voiding cystogram, and occasionally cystoscopy will help to rule out urological abnormalities. If the previous results were negative, the renal biopsy will help to distinguish IgA mesangiopathy, Alport's syndrome or essential hematuria; this last diagnosis resulting by exclusion.
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PMID:[Diagnostic significance of hematuria in pediatrics]. 75 4

A prospective multicenter study was designed to determine the frequency and prognostic importance of hypercalciuria in children with hematuria. Urinary calcium excretion was examined in 215 patients with unexplained isolated hematuria (no proteinuria, urolithiasis, infection or systemic disorder). Hypercalciuria (urinary calcium excretion greater than 4 mg/kg/day) was identified in 76 patients (35%). Compared to patients with normal urinary calcium excretion, children with hematuria and hypercalciuria were characterized by male preponderance, white race, family history of urolithiasis, gross hematuria and calcium oxalate crystals. Renal biopsies were performed in 10 patients with urinary calcium excretion 0.4 to 2.5 mg/kg/day; three had IgA glomerulonephritis, three had glomerular basement membrane thinning, one had proliferative glomerulonephritis and three were normal. Renal biopsies in three patients with hypercalciuria showed focal segmental glomerulosclerosis, hereditary nephritis or no abnormalities. Oral calcium loading tests showed renal hypercalciuria in 26 patients, absorptive hypercalciuria in 15 patients and were not diagnostic in 35 patients. Serum parathyroid hormone, bicarbonate and phosphorus and urinary cyclic adenosine monophosphate concentrations were similar in the three groups of hypercalciuric patients. Urinary calcium excretion after one week of dietary calcium restriction was higher (5.8 mg/kg/day) in renal hypercalciuria than in other hypercalciuric patients (3.4 mg/kg/day), P less than 0.01. One to four years follow-up was available for 184 patients. Eight of 60 hypercalciuric patients developed urolithiasis or renal colic compared to 2 of 124 patients with normal urinary calcium excretion (P less than 0.001). Hypercalciuria is commonly associated with isolated hematuria and represents a risk factor for future urolithiasis in children with hematuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Idiopathic hypercalciuria: association with isolated hematuria and risk for urolithiasis in children. The Southwest Pediatric Nephrology Study Group. 240 91

A retrospective multicentre study of 341 children with persistent/recurrent, isolated haematuria is described. The haematuria was isolated for at least 6 months at the beginning of observation. The duration of follow-up was 2-5 years in 201, 5-10 years in 119, 10-15 years in 19, and over 15 years in 2 cases. Of these patients 47.8% became symptom-free. In 18.4% the haematuria remained isolated; in 13.8% it was combined with proteinuria over 250 mg/day more than 2 years later. The occurrence of associated proteinuria increased progressively with time. It was 8.6% between the 3rd and 5th years, and 37.0% after the 5th year. Renal biopsy was performed because of the symptoms of glomerular disease in 47 cases at an average time of 12 months following the appearance of proteinuria. Proteinuria appeared after a 2-5, 5-10, 10-15 and more than 15 years follow-up period in 16, 23, 6, and 2 patients respectively; 14 of them had Alport's nephropathy. The percentage of more serious azotaemia was 1.7 (creatinine clearance: 10-50 ml/min per 1.73 m2) and 0.3 (creatinine clearance: less than 10 ml/min per 1.73 m2). Mortality was 0.58%. Most of the patients who developed severe azotaemia had persistent microscopic haematuria at the beginning. The prevalence of hypertension was only 1.2%. The time of its appearance was above 5 years in 2 and below 5 years in 2 cases. All these patients had chronic glomerulonephritis. The haematuria was associated with hypercalciuria in 19.9%. In 14.3% of the overall group of patients urolithiasis developed 2-15 years after onset. All of these had hypercalciuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term follow-up of patients with persistent/recurrent, isolated haematuria: a Hungarian multicentre study. 270

A retrospective multicentre study of 341 children with persistent/recurrent, isolated haematuria is described. The haematuria was isolated for at least half a year in the beginning of observation. 47.8% of the patients became symptom-free. In 18.4% the haematuria remained isolated, in 13.8% it was combined with greater than 250 mg/day proteinuria greater than 2 years later. The occurrence of associated proteinuria was 8.6% between the 3rd to fifth years, and 37.0% after the 5th years. 14 cases had Alport's nephropathy. The percentage of more serious azotaemia was 1.7 (Ccreat: 10-50 ml/min/1.73 m2) and 0.3 (Ccreat: less than 10 ml/min/1.73 m2). Mortality was 0.58%, rate of hypertension 1.2%. Most of the patients who developed severe azotaemia, had persistent microscopic haematuria in the beginning. The haematuria was associated with hypercalciuria in 19.9%. In 14.3% of the overall group of patients urolithiasis developed 2-15 years after onset. All of them had hypercalciuria. Our findings suggest that symptoms of isolated haematuria may last for a long-term period and need systematic control. When proteinuria and/or hypertension associates to haematuria a worse prognosis can be expected.
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PMID:[Long-term follow up of chronic recurrent isolated hematuria]. 274 57

A work-up of a child with suspected hematuria should be undertaken once the primary physician has determined that there actually are red blood cells in the urine and that the hematuria is persistent. Evaluation of a child with persistent microscopic hematuria is facilitated with the determination of whether the blood originates from the glomeruli or whether it comes from elsewhere in the urinary tract. Clues to a glomerular origin include the presence of other manifestations of glomerular disease such as significant proteinuria, RBC casts, and dysmorphic erythrocytes in the urinary sediment, hypertension, and renal insufficiency. Clues to the blood originating from the lower urinary tract include blood clots in the urine, normal erythrocyte morphology, and a pertinent history pointing to the lower tract such as that of trauma, urolithiasis, urological or vascular abnormality, or symptoms of bladder inflammation. The initial evaluation should include a detailed patient history and family history as well as a careful physical examination looking for clues to the presence of a familial, hereditary, or chronic kidney disease. A logical, stepwise initial work-up should follow with the goal of ruling out life-threatening and treatable diseases. If there are no indications for immediate further intervention and the cause of the hematuria remains unclear after the initial work-up has been completed, the parents and patient should be reassured that there are no life-threatening conditions and that although the etiology of the blood in the urine is yet unknown, there is time to follow the patient and plan for additional studies if and when they are indicated. The family's concerns (ie, "Is this cancer?," "Will my child require dialysis and transplantation?") should be addressed frankly, and the physician should mention those diagnoses that may lead to renal failure, but have not been absolutely ruled out yet before a kidney biopsy has been performed, such as Alport's syndrome and IgA nephropathy. The child with isolated microhematuria should be evaluated regularly with urinalyses looking for persistence of the hematuria and appearance of proteinuria, blood pressure measurements, and renal function tests. If the microhematuria persists for 6 to 12 months, a kidney biopsy should be considered.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hematuria in children. 780 Apr 21

The ability to predict the rate of progression of renal parenchymal disease may help in its clinical management. We undertook characterization of urinary macrophages obtained from patients with various renal diseases paying special attention to the differentiation from non-progressive to progressive renal diseases. A total of 84 patients were divided into one of three categories. A highly progressive group included patients with rapidly progressive glomerulonephritis, diabetic nephropathy, membranoproliferative glomerulonephropathy, primary focal segmental sclerosis and diffuse proliferative lupus nephropathy, moderately progressive group included those with IgA nephropathy and Alport's syndrome and non-progressive group included patients with thin basement membrane nephropathy, minimal change nephrotic syndrome, idiopathic renal hematuria and urolithiasis. Urinary sediments were reacted with four monoclonal antibodies (CD68/macrophages vimentin, cytokeratin, and 25F9/mature macrophages). In normal individuals mature macrophages (25F9+ cells) were absent in urinary sediments. The number of 25F9+ cells in the urine was highest in the highly progressive group, less prominent in the moderately progressive group, and virtually absent in the non-progressive group. The 25F9+ cells reacted with anti-CD68 and antivimentin antibody, whereas the 25F9+ cells did not react with anti-cytokeratin antibody. These findings indicate that the detection of mature macrophages in urine is useful to estimate the prognosis of renal parenchymal diseases and may help to differentiate some glomerular diseases (e.g., thin basement membrane disease vs. Alport's syndrome, and minimal change nephrotic syndrome vs. primary focal segmental sclerosis).
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PMID:Detection of mature macrophages in urinary sediments: clinical significance in predicting progressive renal disease. 957 70