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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In case of haemolytic uraemic syndrome, it is not always possible to identify on a pure clinical basis the different kidney lesions responsible for the syndrome. We report a series of six cases without thrombotic microangiopathy, which emphasizes the need to perform a kidney biopsy as early as possible, so as to confirm the actual usefulness of plasma exchanges (PE) commonly carried out in emergency in every case of adult haemolytic uraemic syndrome. PATIENTS AND METHODS--Files of patients who were treated for haemolytic uraemic syndrome over the past 14 years were reviewed. Patients in whom thrombotic microangiopathy had been excluded by renal histology data were studied. Every patient was promptly treated with hypotensive drugs, so as to obtain blood pressure levels not exceeding 160-90 mmHg. Dialysis was performed in two patients. Daily PE with fresh frozen plasma were carried out in three patients as early as the first 24 hours after admission, and discontinued immediately after thrombotic microangiopathy could be excluded. RESULTS--All the patients met the usual criteria for diagnosis of haemolytic uraemic syndrome. Elevated liver enzymes were also found in the four cases of preeclampsia, consisting with diagnosis of severe HELLP syndrome. One case was associated with oestrogen therapy. Glomerular lesions were seen in four patients: slight endotheliosis in three cases of preeclampsia; marked lesions of IgA mesangial deposits in the patient who had been treated by contraceptive pill. Three patients had acute tubular necrosis and three had intense lesions of nephrosclerosis. Complete remission was obtained in every case of preeclampsia. Renal failure persisted in two cases (IgA glomerulopathy and one case of nephrosclerosis). DISCUSSION--The histological heterogeneity of haemolytic uraemic syndrome has been already well demonstrated. Typical lesions of thrombotic microangiopathy are usually classified into predominant glomerular lesions, pure arteriolar and mixed lesions. In other cases, thrombotic microangiopathy is not found: kidney lesions may be glomerular (endotheliosis, various subtypes of glomerulonephritis), tubular (acute tubular necrosis) or vascular (nephroangiosclerosis). In every aetiological circumstance, several different lesions may be found together. The usefulness of PE has been proved in thrombotic thrombocytopenic purpura, has been suggested in haemolytic uraemic syndrome and to a lesser extent in persistently severe HELLP syndrome. Unfortunately, none of these reports gave any information about kidney lesions responsible of acute renal failure. CONCLUSION--The haemolytic uraemic syndrome is a syndrome: thrombotic microangiopathy has to be proven when treatment by PE is planned, except in some severe clinical circumstances.
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PMID:A kidney biopsy is clearly mandatory to confirm the indication of plasma exchanges in adult haemolytic uraemic syndrome. 798 52

Acute renal failure occurring in a 24-year-old primigravida with eclampsia and HELLP (hemolysis, elevated liver enzymes, low platelets) syndrome is described. She also had transient disseminated intravascular coagulation. Hemodialysis, fresh blood transfusions, and antihypertensive therapy were administered, and resulted in complete recovery. Kidney biopsy revealed acute tubular necrosis.
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PMID:Acute renal failure in a patient with HELLP syndrome--an unusual complication of eclampsia. 804 68

A retrospective study was done of thirty-patients with severe preeclampsia and HELLP syndrome whose developed acute renal failure, 25 patients also had acute tubular necrosis and five cases bilateral cortical necrosis with chronic renal insufficiency. Severe hypertension was present in all cases and anti-hypertensive therapy was needed. Six patients died, three due to intracranial hemorrhage, other two secondary to hypovolemic shock, and in one case multiple organ dysfunction.
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PMID:[Severe pre-eclampsia, HELLP syndrome and renal failure]. 958 85

Acute renal failure is a rare but serious complication of pregnancy. We describe a 31-year-old woman with haemolytic anemia, elevated liver enzymes, low platelets (HELLP syndrome) who developed acute peripartum renal failure. Renal biopsy performed 2 weeks later because of persistent oliguria revealed thrombotic microangiopathy and acute tubular necrosis. This case highlights the probable pathogenesis of acute renal failure in HELLP patients and explains why it resolves in the majority of cases. A review of the literature that describes renal histology in HELLP patients is presented.
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PMID:Pathogenesis of acute renal failure associated with the HELLP syndrome: a case report and review of the literature. 1269 80

Acute kidney injury (AKI) is costly and is associated with increased mortality and morbidity. An understanding of the renal physiologic changes that occur during pregnancy is essential for proper evaluation, diagnosis, and management of AKI. As in the general population, AKI can occur from prerenal, intrinsic, and post-renal causes. Major causes of pre-renal azotemia include hyperemesis gravidarum and uterine hemorrhage in the setting of placental abruption. Intrinsic etiologies include infections from acute pyelonephritis and septic abortion, bilateral cortical necrosis, and acute tubular necrosis. Particular attention should be paid to specific conditions that lead to AKI during the second and third trimesters, such as preeclampsia, HELLP syndrome, acute fatty liver of pregnancy, and TTP-HUS. For each of these disorders, delivery of the fetus is the recommended therapeutic option, with additional therapies indicated for each specific disease entity. An understanding of the various etiologies of AKI in the pregnant patient is key to the appropriate clinical management, prevention of adverse maternal outcomes, and safe delivery of the fetus. In pregnant women with pre-existing kidney disease, the degree of renal dysfunction is the major determining factor of pregnancy outcomes, which may further be complicated by a prior history of hypertension.
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PMID:Acute kidney injury in the pregnant patient. 2316 15

When a pregnant or postpartum woman presents with sudden and severe microangiopathic hemolytic anemia (MAHA) and thrombocytopenia, three syndromes that require urgent care must be considered: (1) preeclampsia with severe features/hemolysis, elevated liver function tests, low platelets (PE/HELLP) syndrome; (2) thrombotic thrombocytopenic purpura (TTP); and (3) complement-mediated thrombotic microangiopathy (C-TMA; also referred to as atypical hemolytic-uremic syndrome). The distinction among these three syndromes is often unclear because they share multiple clinical features. Overlap between PE/HELLP syndrome and the other two syndromes is also apparent from the fact that pregnancy can be a trigger for both TTP and C-TMA both before and after delivery and also the increased frequency of PE/HELLP syndrome in women who have recovered from TTP. When diagnostic criteria for PE/HELLP syndrome are present, management of hypertension and delivery is curative. Absence of improvement or actual progression of MAHA, thrombocytopenia, and kidney function abnormalities after delivery requires consideration of TTP and C-TMA. Minimal kidney involvement with severe thrombocytopenia suggests TTP and the need for treatment with plasma exchange; progressive kidney injury (in the absence of a cause for acute tubular necrosis) suggests C-TMA and the need for anti-complement treatment. We describe how we use these criteria to evaluate and manage pregnant/postpartum women with MAHA and thrombocytopenia.
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PMID:Syndromes of thrombotic microangiopathy associated with pregnancy. 2663 83