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Query: UMLS:C0451641 (urolithiasis)
 3,973 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

In a prospective study of idiopathic glomerulonephritis we determined the natural history of 49 adult patients (12 primary IgA nephropathy, 13 thin GBM nephropathy, 20 normal renal tissue and 4 miscellaneous nephropathies) who presented with idiopathic non-proteinuric non-azotemic hematuria of at least six months duration, in the absence of hypertension and with a negative urological work-up. The median follow-up was 11 years with a range of 8 to 14 years. At the end of the follow-up, renal function had remained stable in all subsets except for those with miscellaneous disease. Hematuria was still present in all patients with thin GBM nephropathy, in all but two patients with IgA nephropathy who went into immunopathological remission, in three out of four miscellaneous nephropathies, and in seven out of 20 patients with normal renal tissue. Of the latter patients five had a history suggestive of urolithiasis at follow-up, which was in the absence of hypercalciuria and hyperuricosuria. Seven thin GBM patients, five IgA nephropathy patients and three miscellaneous nephropathies developed hypertension; the incidence of hypertension in each subset was significantly higher than in patients with normal renal tissue. This study shows that in young adults with idiopathic chronic non-proteinuric hematuria of four years duration, renal biopsy will give a definite diagnosis in 86% of the patients, and that those patients with so-called minor glomerular diseases are at high risk for hypertension. Those patients with normal renal tissue have a high incidence of urolithiasis and should have a urological follow-up.
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PMID:A prospective study of the natural history of idiopathic non-proteinuric hematuria. 877 Sep 71

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

The renal transplant (Tx) recipient is at risk for developing various complications including urolithiasis, the only manifestation of which may be hematuria. However, there are no data on the prevalence of microscopic hematuria in renal Tx recipients. The objective of our study was to determine the prevalence of microhematuria in our pediatric Tx patients and to investigate the causes of microhematuria. Records of all pediatric renal Tx recipients followed at our center from September 1999 to September 2000 were retrospectively reviewed; of the 21 patients, seven (33%) had persistent microscopic hematuria that was first noted 2.9 years post-Tx. Patients with and without hematuria had similar baseline characteristics. Only one patient had pre-existing hematuria that continued post-Tx. The etiology of hematuria in the other six patients was: recurrent IgA nephropathy (one patient), CMV nephritis (one patient), and unexplained (four patients). None had renal calculi or hypercalciuria. Three of the four patients with unexplained hematuria have chronic allograft nephropathy, and the fourth (original disease dysplasia) has hypocomplementemia. At their last follow-up, 5.3 years after onset of hematuria, all patients are alive with stable allograft function. In conclusion, microscopic hematuria is not uncommon in pediatric renal Tx recipients. While causes of post-Tx hematuria are diverse, stones are not commonly seen. Whether chronic allograft nephropathy per se can be implicated as a cause of hematuria remains to be determined. Renal biopsies should be considered at the onset of hematuria if proteinuria and/or deterioration in renal function are seen concomitantly, to look for recurrent or de novo glomerulonephritis.
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PMID:Microhematuria after renal transplantation in children. 1247 54

Ankylosing spondylitis (AS) affects sacroiliac and axial joints as well as extraarticular organs, such as the eye, lung, bowel, and heart. Although examples of renal involvement in AS, such as IgA nephropathy, amyloidosis, and glomerulonephritis, have been reported, it has not been emphasized that urolithiasis is frequently formed in the clinical course of AS. Growing evidence indicates that urolithiasis may be observed in AS patients and is more frequent than other extraarticular features. In this review, we will discuss frequency and predictors of AS-related urolithiasis and summarize the possible underlying genetic and biochemical mechanisms. We believe an increased awareness of urolithiasis as a complication of AS will encourage future studies that will shed light on disease mechanisms and preventative therapies.
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PMID:Urolithiasis as an extraarticular manifestation of ankylosing spondylitis. 2882 9