Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

IgA nephropathy (IgAN) is an important cause of progressive kidney disease with 25-30% of patients developing end-stage renal disease within 20 years of diagnosis. There is still no treatment to modify mesangial IgA deposition and available treatments are those extrapolated from the management of other patterns of chronic glomerulonephritis. There remains no consensus on the use of immunosuppressive agents for treatment of progressive IgAN and this is compounded by the relative lack in IgAN of randomized controlled trials relevant to current clinical practice. Patients with recurrent macroscopic hematuria or isolated microscopic hematuria and proteinuria <1 g/24 h require no specific treatment. Those with nephrotic syndrome and minimal change on renal biopsy should be managed as for minimal change nephropathy. There is no evidence to support the use of corticosteroids for nephrotic IgAN outside this group of patients. Patients presenting with acute renal failure require evaluation to distinguish acute tubular necrosis, which requires supportive therapy only, from crescentic IgAN, for which treatment with cyclophosphamide and corticosteroids in a regimen similar to that for renal small vessel vasculitis is indicated in the absence of significant chronic histologic injury. Patients at greatest risk of progressive renal impairment are those with hypertension, proteinuria >1 g/24 h, and reduced glomerular filtration rate at diagnosis. All such patients should be treated to a blood pressure of 125/75 mm Hg with dual blockade of the renin-angiotensin system with angiotensin-converting enzyme inhibition and angiotensin receptor blockade. At present, there is insufficient evidence for the additional use of immunosuppressive agents, antiplatelet agents, or anticoagulants.
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PMID:Treatment of IgA nephropathy. 1705 Dec 61

Acute renal failure is a known complication during hemolytic crisis in paroxysmal nocturnal hemoglobinuria (PNH). However, chronic renal failure is rare despite the well-known spectacular hemosiderosis of the kidneys due to chronic hemolysis. Here, we report about a 74-year-old man with PNH who developed acute on chronic renal failure after an episode of intercurrent urinary tract infection and subsequent hemolytic crisis. Mild chronic hemolysis, well-documented over the past decade, had long been considered the cause of a constantly declining glomerular filtration rate. Accordingly, magnetic resonance imaging during admission demonstrated marked siderosis of both kidneys, supporting the hypothesis that chronic renal failure (CRF) was likewise related to PNH. However, a renal biopsy revealed acute tubular necrosis and distinct renal siderosis, as expected. Additionally, tubulointerstitial injury and global glomerular sclerosis, best classified as arterionephrosclerosis, were present. In retrospect, these findings were explained by a 15-year history of hypertension and a 4-year medication with cyclosporine. Careful diagnostic workup including a renal biopsy is mandatory, given a misleadingly suggestive correlation between chronic hemolysis and CRF. Chronic renal failure in PNH is a diagnosis of exclusion, even if radiologic evidence of heavy siderosis draws off the physician's attention.
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PMID:A blue kidney--chronic renal failure as a consequence of siderosis in paroxysmal nocturnal hemoglobinuria? 1699 44

HIV-infected patients may undergo renal damage related to the HIV infection itself, to the presence of co-infections, arterial hypertension, diabetes or to the exposure to nephrotoxic drugs. Tenofovir has been associated with the development of acute renal failure with Fanconi syndrome and acute tubular necrosis and, albeit rarely, with chronic liver disease. Patients with low CD4 cell count, low body weight and with concomitant diseases such as arterial hypertension and diabetes or co-infections with HCV, HBV or Treponema pallidum seem at higher risk of tenofovir-related nephrotoxicity. Other risk factors include previous exposure to nephrotoxic drugs and the association of tenofovir with boosted protease inhibitors or with didanosine. However, from the analysis of published papers the incidence of tenofovir-related renal toxicity seems low, as confirmed also by our personal casuistry (SCOLTA Project). Thus, a careful selection of patients including the evaluation of existent renal disease before starting an antiretroviral regimen including tenofovir is necessary to prevent renal damage. Furthermore, frequent monitoring of renal function in patients at higher risk of renal damage is strongly recommended, as well as a tenofovir dose adjustment if an alteration of renal function is detected.
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PMID:[Renal toxicity in HIV-infected patients receiving HAART including tenofovir]. 1712 26

Elderly individuals comprise the faster growing patient population group and acute renal failure (ARF) is quite common among them, although exact numbers are not known. We reviewed the literature with regards to the characteristics of ARF in elderly patients and describe some useful guidelines. The ageing kidney is characterized by many structural and functional changes, which are mainly due to various chronic disorders, such as hypertension, diabetes and atherosclerosis, which are highly prevalent in these patients. A number of structural and functional changes characteristic of the ageing kidney make elderly people especially prone to renal damage. ARF in the elderly is frequently of multifactorial origin and often with an atypical presentation, like the "intermediate syndrome", which combines characteristics of pre-renal azotemia and acute tubular necrosis. Physical examination and laboratory blood and urine indices may sometimes be misleading occasionally leading to misdiagnosis. Prophylaxis remains the preferred approach to therapy: one should avoid nephrotoxic drugs and poly-pharmacy, adjust drug doses and achieve adequate hydration of the patient as cautiously as possible. Dialysis therapies can be used for treatment of ARF irrespective of age and carry a good prognosis.
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PMID:Acute renal failure in the elderly: particular characteristics. 1716 Jun 31

Over a ten year period (1979 to 1989), 200 patients have undergone live donor nephrectomy through a flank extraperitoneal approach without rib resection. The average hospital stay was short and the major complications were negligible. Early graft function was seen in 97% of the cases. Delayed function due to acute tubular necrosis developed in 3%. Urinary leak was seen in 3%. Two kidneys were lost due to infection related to urinary fistulate. In 70 donors, 37 +/- 13 month's follow-up was available. Hypertension developed in two patients three and three and one-half years post donation. Significant proteinuria (>300 mg/day) was noted in one patient. No significant renal functional abnormalities were observed. Creatinine clearance was about 70% of the initial measurement at the observation time. We conclude that extraperitoneal flank live donor nephrectomy is generally safe and associated with minimal perioperative and long-term morbidity. Moreover, the procedure provides an excellent allograft function.
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PMID:Experience with living related donor nephrectomy: Evaluation of 200 cases. 1759 Jul 20

To determine the conditions that result in pediatric nephrology consultations in an academic hospital setting, we studied 178 prospective consecutive consultations for 125 inpatients (69 boys and 56 girls) at the Jordan University Hospital, Amman, Jordan from January 2006 to December 2006. The mean age at the time of consultation was 3.1 years (median of 1 year, and range from 1 day to 16 years). Of the 125 patients, 87 (69.6%) patients had a single consultation, while 38 (30.4%) patients had multiple encounters (range from 1-4 consultations). The reasons for consultations included fluids and electrolytes imbalances (29.0%), hydronephrosis (15.7%), urinary tract infections (14.2%), acute renal failure (ARF) (14.2%), hypertension (8.40%), and miscellaneous conditions (18.5%). The most frequent fluids and electrolyte disorders were polyuria, hypocalcemia, and hyponatremia. Routine administration of hypotonic intravenous fluids was a major contributory factor to hyponatremia. The most frequent cause of ARF was acute tubular necrosis in association with multiple organ dysfunction and antibiotic nephrotoxicity. Hypertension was mostly neurogenic in origin.
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PMID:Pediatric nephrology consultations in a tertiary academic center in Jordan. 1844 13

Current clinical requirements mandate the existence of a renal diuretic protocol, which is fast and easy, applicable in all ages and for all indications, convenient for both the patient and the technologist, and provides diagnostic as well as prognostic information. Seventeen years ago a 25-minute protocol, after oral hydration, with no bladder catheterization, and simultaneous injection of mercapto-acetyl-triglycine (MAG(3)) and furosemide (MAG(3)-F(0)), was initiated. It initially was used for the evaluation of drainage and emerged as a protocol to also evaluate the renal parenchyma. Results of this protocol have been published individually, per clinical application. MAG(3)-F(0) was instrumental in the evaluation and prognosis of congenital disorders. For obstruction, in the newborn, an increasing renogram mandates intervention, whereas a downsloping one predicts spontaneous resolution. In children or adults, preoperatively or postoperatively, when the cortex was visualized and drained normally, there was no obstruction, even if urine was retained within a dilated collecting system or an extrarenal pelvis. For diseases of the renal parenchyma, the protocol enabled the diagnosis of acute pyelonephritis (APN) revealing the "regional parenchymal dysfunction," diagnostic of APN. Diffuse parenchymal diseases were characterized by increased residual cortical activity (RCA), and their progression was manifested as a deterioration of RCA. End-stage renal disease was characterized by lack of accumulation and retention. Trauma and leaks were identified with specific patterns. In renovascular hypertension (RVH), an increase in RCA after angiotension-converting enzyme inhibitors is diagnostic of RVH and prognostic of the beneficial effect of angioplasty on hypertension. In renal colic, stratification was possible into (1) complete or severe obstruction requiring immediate intervention, (2) mild obstruction allowing waiting, (3) spontaneous decompression (stunned kidney), and (4) no recent obstruction. In transplants, it enabled differentiation of acute tubular necrosis, acute or chronic rejection and nephrotoxicity, and identified infarcts, RVH, leaks and obstruction. Finally, this method allows for a quick semiquantification of renal function. The clinical usefulness of the MAG(3)-F(0) protocol in most congenital or acquired renal problems is proven through long-term clinical experience and has resulted in a substantial utilization of the test at our Center.
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PMID:A renal protocol for all ages and all indications: mercapto-acetyl-triglycine (MAG3) with simultaneous injection of furosemide (MAG3-F0): a 17-year experience. 1934 36

It is now clearly established that anti-vascular endothelial growth factor (VEGF) drug class induces hypertension and proteinuria sometimes related to thrombotic microangiopathy and/or various glomerulopathies, according to capillary and glomerular VEGF and VEGF-receptor expressions. As reported in the literature, anti-epidermal growth factor receptor (EGFR) therapies seem to be less nephrotoxic. Indeed, many reports of anti-EGFR nephrotoxicity are tubular dependent such as acute tubular necrosis, electrolyte disorders (hypophosphatemia, hypomagnesemia, etc.) or both. This is explained by elective tubular expression of renal EGF/EGFR. In this paper, we focus on electrolyte disorders related to anti-EGFR treatment and discuss the tubular involvement of these drugs based on their renal expression.
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PMID:Electrolyte disorders related to EGFR-targeting drugs. 1940 15

The prognostic of uremic syndrome had been improved by the development of renal replacement therapy. Uremic syndrome remains a dramatic medical concern in African sub-saharan countries. Nephrology practice has been introduced recently in Burkina Faso and epidemiological data on acute renal failure is not available. We conducted this study with the aim to describe the clinical profile of hospitalized patients. One hundred and twenty-one patients (18.4% of all admissions) with acute renal failure (creatinine>240micromol/L, abrupt onset) were included (age: 38.6+/-16.3y; creatinine: 1246.1+/-870.5micromol/L; urea: 40.2+/-18.3micromol/L), 75 men (age: 41.2+/-16.4) and 46 women (age: 34.2+/-15.2y). Acute renal failure was of medical cause in 91 cases, surgical cause in 16 cases and gyneco-obstetrical in 14 cases. Many pathophysiological factors have been identified like volume depletion, infections and obstruction. Acute renal failure was renal in 57 cases (age: 38.2+/-14.6y), prerenal in 43 cases (age: 36.8+/-16.7y) counting acute tubular necrosis in 21 cases, obstructive in 15 cases (age: 50.5+/-15.6y) and unclassified in six cases. Comorbidities have been identified: heart failure (13 cases), hepatocellular failure (eight cases), tumours (four cases) and severe hypertension (13 cases). Dialysis was justified in 84 cases but only accomplished in 14 cases. Hospital length of stay was 20.4+/-14.9 days. Twenty-nine patients died and causes were uraemia in 13 cases, hepatic in three cases, sepsis in 10 cases, malignant tumour in two cases and associated in one case.
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PMID:[Acute renal failure in Burkina Faso]. 1983 24

During normal pregnancy, renal blood flow and GFR increase gradually until they reach a peak of about 150% of their normal values by the end of the 1(st) trimester. This increase in GFR is secondary to the extra-cellular compartment expansion caused by a positive sodium balance of about 500-900 mmol which is in turn associated with a water retention amounting 6 to 8 liters. Blood pressure decreases during a normal pregnancy because of the decrease in peripheral vascular resistance. This drop in blood pressure is limited by the renin-angiotensin system. Blood pressure gradually recovers during the 3(rd) trimester. Systemic hypertension, proteinuria >0.3 g/day and edema are the usual signs leading to the diagnosis of PE. However, any of the above listed signs found in isolation can be a tell tale sign of PE and must therefore prompt for the identification of a possible fetal effect The differential diagnosis of PE includes essential hypertension and hypertension secondary to a pre-existing renal failure. In the latter, signs of renal impairment early in the pregnancy, or (and) renal failure prior to the pregnancy are of important diagnostic clues. Causes of acute renal failure during pregnancy are numerous. PE associated acute renal failure presents in 5-10% of severe forms of PE. This is always a bad prognostic sign with a predicted mortality of 10%. Histological features are those of acute tubular necrosis with "endotheliosis" an inflammation of the glomerular endothelium. This renal impairment is frequently complicated by pulmonary edema. Passed the acute phase, the recovery of the renal function is usually complete. An acute renal failure during pregnancy can also be secondary to a pre-existing renal impairment suddenly aggravated by PE. In this setting, the probability of these patients requiring long term dialysis is high. Post-partum Haemolytic-Uremic Syndrome (HUS), although rare, is a serious condition which, following delivery, will require an early diagnosis (haemolysis, hypertension, acute renal failure) and urgently require symptomatic, perhaps specific, treatment (Plasma exchange transfusion).
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PMID:[Kidney and preeclampsia]. 2035 4


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