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)

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 case of idiopathic interstitial nephritis who underwent to chronic renal failure without history of hematuria nor proteinuria is discussed. A 46 years old woman who showed gradually elevation of serum creatinine (1.3-2.5 mg/dl) admitted on our hospital. On occasions of pregnancy, health examination or hospital visit, she has never been pointed out hematuria nor proteinuria. Immunological disorders such as SLE, metabolic diseases, urinary tract obstruction and chronic urinary tract infection were excluded by the examinations after admission. Because of the severe enzymuria (beta 2-microglobulin, N-acetyl glucosaminidase), chronic interstitial nephritis was considered, and renal biopsy was performed. Severe tubulointerstitial changes were observed histologically, however, glomerular damage was comparatively mild. From these results, she was diagnosed idiopathic chronic tubulointerstitial nephritis. In this case, hematuria and proteinuria were absent until severe renal dysfunction. This may be caused by that inflammation was located to the tubulointerstitial area. The observation of enzymuria seemed to be important to diagnosis and follow-up of the interstitial nephritis.
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PMID:[A case of idiopathic chronic interstitial nephritis progressed to renal failure without proteinuria nor hematuria]. 158 74

213 patients with urinary schistosomiasis were investigated under field conditions in the Peoples Republic of Congo by quantitative parasitological examination, urine analysis and abdominal ultrasonography. The study group consisted mainly of children. Disease related pathological ultrasonographical findings were dependent on the intensity of infection. Sixty patients had bladder wall thickening and 55 patients had vesical polyps. Those with multiple vesical polyps were the only patients with urinary retention and they had a significantly higher proteinuria than those with a singular polyp. Obstructive uropathy of different degrees was encountered in 50 cases. Of these, 21 patients had moderate to severe urinary tract obstruction and in all cases except one also presented concomitant vesical abnormalities. Nine patients revealed bilateral obstructive uropathy. Lesions of the lower urinary tract were a predisposing factor in the development of urinary tract obstruction. Morbidity of study patients was considered to be substantial. A proteinuria of more than one gramme per litre in spontaneously voided midday urine indicated a high probability for the presence of urinary tract obstruction and was considered an urgent indication for antischistosomal treatment.
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PMID:Morbidity in urinary schistosomiasis: relation between sonographical lesions and pathological urine findings. 393 56

Renal changes that occur with aging mainly consist of impairment in the ability to concentrate urine and to conserve sodium and water. These physiological changes increase the risk of volume depletion and the prerenal type of acute renal failure (ARF) in elderly people. Bladder outlet obstruction caused by benign prostatic hypertrophy is a common cause of ARF in elderly men. Another frequent cause of ARF in the elderly is drug-induced nephropathy. Nonsteroidal anti-inflammatory drugs (NSAIDs) and antibiotics are most often implicated in the development of ARF in the elderly. However, considering the high usage of these drugs, the incidence of drug-induced nephropathy is relatively small. NSAIDs are more likely to cause ARF in patients with congestive heart failure, chronic renal disease (including diabetic nephropathy) or chronic liver disease than in otherwise healthy individuals. NSAID-induced ARF is often of the prerenal type, but may be caused by acute interstitial nephritis (AIN). The presence of heavy proteinuria or nephrotic syndrome differentiates NSAID-induced AIN from AIN caused by other drugs. Antibiotics, especially semisynthetic penicillins, more commonly give rise to AIN associated with peripheral blood eosinophilia and eosinophiluria than NSAIDs. Ciprofloxacin is increasingly reported to cause AIN. Fever commonly accompanies AIN, especially when induced by antibiotics. Aminoglycosides produce ARF by inducing acute tubular necrosis (ATN), which results from the excessive accumulation of myeloid bodies in the tubules. In all cases of ARF it is essential to obtain a good history, to perform a through physical examination, with particular attention to skin turgor, and to measure blood pressure, pulse rate (supine and upright), urinary electrolyte and creatinine levels. Fractional excretion of sodium and the urine:plasma creatinine ratio are reliable indices that distinguish prerenal ARF from ATN. A prompt response to fluid challenge, with an increase in urine output and urinary sodium excretion, and a rapid decrease in blood urea nitrogen, constitutes strong evidence for prerenal ARF. However, these indices are unreliable when prerenal ARF has progressed to ATN or when ARF has an obstructive pattern to begin with. In all cases of ARF, especially in elderly men, urinary tract obstruction should be suspected unless the history is otherwise clear cut. Ultrasound of the kidneys and bladder is a simple, non-invasive and meaningful test that can be used to rule out obstructive causes of ARF. If obstruction is the cause of ARF, ultrasound will be positive; in contrast, urinary obstruction is very unlikely if ultrasound findings are normal in a patient who has been oliguric or anuric for 48 hours or more. Similarly, acute glomerulonephritis, including rapidly progressive glomerulonephritis, should be suspected when ARF is associated with heavy proteinuria. In such instances, percutaneous renal biopsy is essential to document the diagnosis. It is of utmost importance to establish whether ARF is of prerenal or postrenal type, both of which are potentially fully reversible. In contrast, patients with ATN or rapidly progressive glomerulonephritis may not recover, or may only partially recover, their renal function. Haemodialysis and nutritional support are common measures for patients with severe ATN and a highly catabolic state. Corticosteroids and immunosuppressive therapy should be instituted for rapidly progressive glomerulonephritis, in addition to haemodialysis. haemodiafiltration instead of haemodialysis is recommended for patients who are haemodynamically unstable [i.e., with a persistently low blood pressure (systolic < or = 100 mm Hg)]. Haemodiafiltration has been shown to improve acid-base balance and uraemia better than standard haemodialysis. However, despite dialysis, mortality in patients with ARF associated with ischaemic ATN remains high.
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PMID:Management of acute renal failure in the elderly. Treatment options. 889 22

Health questionnaires and parasitologic examinations of urine and stool were performed upon a stratified random sample of 7,710 individuals from 1,109 households in 21 rural communities in Fayoum Governorate, Egypt in 1992 to investigate the prevalence of, risk factors for, and changing pattern of, infection with Schistosoma sp. in the governorate. A subset, every fifth household, or 1,038 subjects, had physical and ultrasound examinations to investigate prevalence of, and risk factors for, morbidity. The prevalence of S. haematobium ranged from 0% to 27.1% and averaged 13.7%. The geometric mean egg count (GMEC) was 10.0 eggs/10 ml of urine. Age-stratified prevalence and intensity of infection were 18-25% and 10-15 eggs/10 ml of urine in those 5-25 years of age. Schistosoma mansoni were detected in inhabitants of 13 communities, but 78.5% of the infections were focally present in a group of 4 satellite hamlets around a single village. The overall prevalence of S. mansoni in the governorate was 4.3% and the GMEC was 44.0 ova/g of stool. Risk factors for infection with either species were male gender, an age <20 years, living in smaller communities, and exposures to canal water by males. Histories of burning micturation, blood in the urine, or prior schistosomiasis and reagent strip-detected hematuria and proteinuria were risks for S. haematobium, but not for S. mansoni. Both urinary tract and higher grades of hepatic morbidity were rare. Obstructive uropathy was present in 6.3% of the subjects and was more common in males and older people. Ultrasonography-detected bladder lesions were present in 5.2% and correlated with S. haematobium only in younger subjects and in those with hematuria and proteinuria. The prevalences of hepatomegaly, splenomegaly, and periportal fibrosis (PPF) were associated with each other and increased with age and in males. Ultrasonography-detected hepatomegaly and splenomegaly were weakly associated with S. mansoni infections only in children. The prevalence of PPF was greater in the 4 communities with >25% S. mansoni infection rates in comparison with the 17 other villages and ezbas. Transmission of S. mansoni is focally well established in Fayoum, which also has the highest prevalence of S. haematobium in the governorates surveyed by the Epidemiology 1, 2, 3 Project. However, both urinary tract and hepatic morbidity are relatively rare in the governorate. This probably results from the long-standing schistosomiasis control program in Fayoum, which suppressed intensity more than prevalence of infection, leading to less community morbidity.
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PMID:The epidemiology of schistosomiasis in Egypt: Fayoum Governorate. 1081 1

Nephrotoxicity is an inherent adverse effect of certain anticancer drugs. Renal dysfunction can be categorised as prerenal uraemia, intrinsic damage or postrenal uraemia according to the underlying pathophysiological process. Renal hypoperfusion promulgates prerenal uraemia. Intrinsic renal damage results from prolonged hypoperfusion, exposure to exogenous or endogenous nephrotoxins, renotubular precipitation of xenobiotics or endogenous compounds, renovascular obstruction, glomerular disease, renal microvascular damage or disease, and tubulointerstitial damage or disease. Postrenal uraemia is a consequence of clinically significant urinary tract obstruction. Clinical signs of nephrotoxicity and methods used to assess renal function are discussed. Mechanisms of chemotherapy-induced renal dysfunction generally include damage to vasculature or structures of the kidneys, haemolytic uraemic syndrome and prerenal perfusion deficits. Patients with cancer are frequently at risk of renal impairment secondary to disease-related and iatrogenic causes. This article reviews the incidence, presentation, prevention and management of anticancer drug-induced renal dysfunction. Dose-related nephrotoxicity subsequent to administration of certain chloroethylnitrosourea compounds (carmustine, semustine and streptozocin) is commonly heralded by increased serum creatinine levels, uraemia and proteinuria. Additional signs of streptozocin-induced nephrotoxicity include hypophosphataemia, hypokalaemia, hypouricaemia, renal tubular acidosis, glucosuria, aceturia and aminoaciduria. Cisplatin and carboplatin cause dose-related renal dysfunction. In addition to increased serum creatinine levels and uraemia, electrolyte abnormalities, such as hypomagnesaemia and hypokalaemia, are commonly reported adverse effects. Rarely, cisplatin has been implicated as the underlying cause of haemolytic uraemic syndrome. Pharmaceutical antidotes to cisplatin-induced nephrotoxicity include amifostine, sodium thiosulfate and diethyldithiocarbamate. Dose- and age-related proximal tubular damage is an adverse effect of ifosfamide. In addition to renal wasting of electrolytes, glucose and amino acids, Fanconi syndrome, rickets and osteomalacia have occurred with ifosfamide treatment. High dose azacitidine causes renal dysfunction manifested by tubular acidosis, polyuria and increased urinary excretion of electrolytes, glucose and amino acids. Haemolytic uraemia is a rare adverse effect of gemcitabine. Methotrexate can cause increased serum creatinine levels, uraemia and haematuria. Acute renal failure is reported following administration of high dose methotrexate. Urinary alkalisation and hydration confer protection against methotrexate-induced renal dysfunction. Dose-related nephrotoxicity, including acute renal failure, are reported subsequent to treatment with pentostatin and diaziquone. Acute renal failure is a rare adverse effect of treatment with interferon-alpha. Haemolytic uraemic syndrome occurs with mitomycin administration. A mortality rate of 50 to 100% is reported in patients developing mitomycin-induced haemolytic uraemic syndrome. Capillary leak syndrome occurring with aldesleukin therapy can cause renal dysfunction. Infusion-related hypotension during infusion of high dose carmustine can precipitate renal dysfunction.
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PMID:Anticancer drug-induced kidney disorders. 1121 85

Renal damage in children has been found to be more congenital in origin than was previously thought. Congenital anomalies of the kidney and urinary tract (CAKUT) involve renal dysplasia, renal hypoplasia, urinary tract obstruction and vesicoureteral reflux. CAKUT are sometimes bilateral and different types often coexist. Depending on their types and severity, children with CAKUT often have varying degrees of a reduced number of nephrons at birth. CAKUTare now the leading cause of renal failure in children. Children with renal dysplasia or obstructive uropathy may have abnormal renal tubules, and tend to lose essential water and sodium in urine. This can lead to poor body growth unless they are supplemented with water and sodium. Children with severe ureteric reflux often develop urinary infection and renal scarring. Renal scarring can further increase the risk of renal failure in children who already have other CAKUTand fewer nephrons than normal. Hypertension and proteinuria may develop in children with renal dysplasia and further aggravate renal function unless they are treated. Recent advances in the understanding and management of CAKUT make it possible for children with CAKUT to grow normally, have fewer complications such as urinary infection, have longer renal survival, and survive even with end-stage renal diseases through renal replacement therapy.
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PMID:Medical management of congenital anomalies of the kidney and urinary tract. 1452 48

Significant advances have been made recently in elucidating the cellular consequences of urinary tract obstruction during renal development. Urinary tract obstruction impairs growth and maturation of the kidney, and can also cause renal maldevelopment. This includes a reduction in the number of nephrons, tubular atrophy, and progressive interstitial fibrosis. Apoptosis (programmed cell death) accounts for much of the loss of tubular epithelial cells. Factors contributing to apoptosis include stretching of cells in dilated tubules, altered renal production of growth factors, and infiltration of the renal interstitium by macrophages. Two major controversies remain regarding the surgical management of congenital obstructive nephropathy: first, which fetuses with bladder outlet obstruction should undergo prenatal intervention, and second, which infants should undergo early pyeloplasty for ureteropelvic junction obstruction? Even after successful surgery for congential obstructive nephropathy, all patients should be followed for hypertension, proteinuria, or renal deterioration.
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PMID:Perinatal obstructive nephropathy. 1520 Feb 51

The acute renal failure is a grave pathology, of rapid establishment and relatively frequent in the hospital environment. We can describe three etiological groupS, which are responsible for it, amongst which are emphasized the pre-renal reasons. The obstructive pathology, of minor incidence, increases with the age. It is described the case of a 67-yr-old patient who was admitted in the Nephrology Service because of abrupt decline of the renal function. Among the initial symptoms, he presented arterial hypertension (190/90) and preserved diuresis. Blood analysis: urea 199 mg/dl, creatinine 7.7 mg/dl, without proteinuria. Sonography reported a bilateral ureteral hydronephrosis with simple cyst of possible ischemic origin. In view of the absence of previous biochemical data of renal failure, we considered possible reasons which start with an acute pattern. In initial evaluation, pre-renal etiology was not seen (high blood pressure, right cardiac systole function). The absence of prostatic syndrome and sonography discovery did not justify a diagnosis of urinary tract obstruction. Finally, abdominal-pelvic scan showed a periaortic retroperitoneal mass which included both ureters and appeared to trigger the obstruction. Combined efforts were pursued with the Urology Service, which implanted a bilateral "double J" catheter and later operated surgically on the patient, carrying out an alternating ureterolysis of both ureters. The biopsy manifested a retroperitoneal fibrosis, and the renogram showed a residual renal function of 20% in the right kidney and 80% in the left kidney. Due to the failure of the previous measures and as a last therapeutic recourse when one year had passed from the diagnosis, a continuous regimen with tamoxifen (anti-estrogen drug) in dose of 20 mg/dl each 12 hours was started, which began a progressive remission in the size of the observed mass by scan (CT) and magnetic resonance (MR). The treatment was completed during 12 months and in this time, the levels of blood urea nitrogen and creatinine were reduced gradually too. Finally, at the end of the treatment, the magnetic resonance demonstrate the complete disappearance of the fibrosis.
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PMID:[Acute obstructive renal failure secondary to retroperitoneal mass]. 1521 69

Long-term allograft survival poses a major problem in pediatric renal transplantation, with allograft nephropathy being the principal cause of graft failure after the first post-transplant year. The mechanisms of nephron loss resulting in graft dysfunction are multiple, comprising both immunologic factors such as acute and chronic antibody- or T-cell-mediated rejection and non-immunologic components. The latter include peri-transplant injuries and renovascular lesions (renal artery stenosis, thrombosis) as well as cardiovascular risk factors such as arterial hypertension and hyperlipidemia. Another relevant issue leading to progressive nephron loss and declining kidney transplant function is acute and chronic nephrotoxicity induced by the calcineurin inhibitors (CNIs) ciclosporin (cyclosporine microemulsion) and tacrolimus. Furthermore, the presence of an abnormal lower urinary tract as well as bacterial (recurrent pyelonephritis) and viral (cytomegalovirus [CMV], polyomavirus [BK virus; BKV]) infections are crucial factors involved in the incidence of chronic allograft dysfunction and graft failure. Renovascular lesions and lower urinary tract obstruction are typical indicators for surgical intervention. The aim of treatment in pediatric patients with renal failure secondary to a dysfunctional lower urinary tract is to create a sterile, continent, and nonrefluxive reservoir. Surgical techniques such as bladder augmentation and the introduction of intermittent catheterization and anticholinergic therapy have significantly improved graft outcome. Arterial hypertension, another factor responsible for graft function deterioration in pediatric renal transplant recipients, is controlled preferably by the use of angiotensin converting enzyme (ACE) inhibitors or angiotensin II receptor antagonists, which are known to possess nephroprotective properties in addition to their potent antihypertensive effects. Although treatment of subclinical rejection with augmented immunosuppression has been associated with better graft survival, an increase of the immunosuppressive level to avoid subclinical rejection should be weighed against the risk of infection. The majority of viral infections affecting kidney allografts are caused by CMV and BKV. Antiviral CMV prophylaxis or pre-emptive therapy with ganciclovir has been shown to have beneficial effects in the pediatric renal transplant population. Treatment of BKV-induced nephropathy is based on reduction of the immunosuppressant therapy, although specific antiviral agents such as cidofovir and leflunomide are known to inhibit BKV. However, cidofovir itself is nephrotoxic and should therefore be administered cautiously to pediatric renal transplant patients. Since CNIs are likewise known for their nephrotoxic effects, especially with long-term use, alteration of the immunosuppressant regimen is necessary in case of deteriorating graft function due to CNI-induced histopathologic changes. Complete CNI avoidance seems inappropriate because, in this situation in pediatric renal transplant recipients, other relatively potent immunosuppressant agents such as lymphocyte-depleting antibodies, which are frequently accompanied by a higher incidence of infections, are needed for rejection prophylaxis. CNI withdrawal and switching of the immunosuppressant regimen from CNI therapy to sirolimus may be an option for some pediatric renal transplant patients with less advanced graft function deterioration. Nevertheless, potential adverse events such as aggravation of proteinuria, hyperlipidemia, myelosuppression, and hypergonadotropic hypogonadism have to be considered, and controlled studies are lacking. At present, an immunosuppressant maintenance therapy composed of low-dose tacrolimus or ciclosporin (CNI minimization) and mycophenolate mofetil with low-dose corticosteroids appears to be the most promising strategy to adopt in pediatric renal transplant recipients at low or normal immunologic risk.
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PMID:Treatment strategies to minimize or prevent chronic allograft dysfunction in pediatric renal transplant recipients: an overview. 1987 24


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