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 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In the following we describe a case of nephropathia epidemica, which exhibited, a few years after acute infection, arterial hypertension and multiple papillary necrosis. Papillary necrosis was diagnosed by i.v. pyelography and CT Scan. A complete evaluation of the patient failed to show any other etiology for medullary necrosis. If arterial hypertension has already been reported as a complication of nephropathia epidemica, papillary necrosis is exceptional, but may be explained by the severe vascular troubles engendered by Hantavirus infection in kidney medulla.
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PMID:Papillary necrosis: a late complication of nephropathia epidemica? 935 63

Sickle cell anemia and the related hemoglobinopathies are associated with a large spectrum of renal abnormalities. The patients have impaired urinary concentrating ability, defects in urinary acidification and potassium excretion, and supranormal proximal tubular function. The latter is manifest by increased secretion of creatinine and by reabsorption of phosphorus and beta(2)-microglobulin. Young patients with sickle cell disease (SCD) have supranormal renal hemodynamics with elevations in both effective renal plasma flow (ERPF) and glomerular filtration rate (GFR). These parameters decrease with age as well as following the administration of prostaglandin inhibitors. Proteinuria, a common finding in adults with sickle cell disease, may progress to the nephrotic syndrome. Proteinuria, hypertension, and increasing anemia predict end-stage renal disease (ESRD). While ESRD can be managed by dialysis and/or renal transplantation, there may be an increased rate of complications in renal transplant recipients with SCD. Hematuria is seen in individuals with all of the SCDs as well as with sickle cell trait. In most cases the etiology of the hematuria turns out to be benign. However, there does appear to be an increased association between SCD and renal medullary carcinoma. Therefore, those SCD patients who present with hematuria should initially undergo a thorough evaluation in order to exclude this aggressive neoplasm. Papillary necrosis may occur due to medullary ischemia and infarction. Erythropoietin levels are usually lower than expected for their degree of anemia and decrease further as renal function deteriorates. An abnormal balance of renal prostaglandins may be responsible for some of the changes in sickle cell nephropathy. Acute renal failure is a component of the acute multiorgan failure syndrome (MOFS). Finally, progression of sickle cell nephropathy to ESRD may be slowed by adequate control of hypertension and proteinuria. However, the prevention of the renal complications of SCD will require a cure for this genetic disorder.
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PMID:Renal abnormalities in sickle cell disease. 1142 1

Selective cyclooxygenase 2 (COX-2) inhibitors are known to affect renal prostaglandins (epoprostenol and dinoprostone), which are at least in part COX-2 dependent. Consequently, adverse events including hypertension, peripheral edema, hypercalemia, hyponatremia, and acute renal failure have been reported to occur with the new COX-2-specific inhibitors. This case report posits celecoxib as a likely cause of renal papillary necrosis and alerts physicians to the possibility of this additional renal complication with COX-2-specific inhibitors.
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PMID:Celecoxib-related renal papillary necrosis. 1252 25

A 60-year-old lady with type 2 diabetes mellitus and hypertension was referred for fever, bilateral loin pain, and renal failure. Investigations showed severe acute renal failure, bilateral renal papillary necrosis (RPN), urinary tract infection (E. coli), and infection with leptospirosis: Leptospira icterohemorrhagica; serovar hardjo. Renal biopsy showed tubulointerstitial nephritis with mesangial proliferation. The diagnosis was bilateral RPN in a diabetic lady with acute renal failure due to leptospirosis. The patient was successfully treated with hemodialysis, injection ceftriaxone, and benzyl penicillin.
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PMID:Reversible acute kidney injury due to bilateral papillary necrosis in a patient with leptospirosis and diabetes mellitus. 2332 55

This is a case of idiopathic pulmonary calcification and ossification in a 70 year old with long-standing diabetes and hypertension. Thirteen years prior to her demise, she was first noticed to have multiple calcific deposits in her lungs on a chest X-ray film. She had no risk factors for soft tissue calcification and ossification. Histology of tissue from autopsy showed intraparenchymal pulmonary calcification and ossification with marrow elements. Idiopathic pulmonary calcification and ossification is rare. At autopsy, she was also found to have had bilateral subarachnoid haemorrhage (SAH), a diagnosis missed during clinical evaluation. We highlight the pertinent details in our patient's management that could have helped to prevent a missed diagnosis of SAH. Even though SAH occurs most commonly following head trauma, the more familiar medical use of SAH is for non-traumatic SAH occurring following a ruptured cerebral aneurysm. This patient had notable risk factors for cerebral aneurysm formation but an aneurysm was not identified at autopsy. The location of the blood high on the cerebral convexities further suggests a traumatic origin rather than a ruptured aneurysm. Heterotopic calcification and ossification (HO) is known to occur in the setting of severe neurologic disorders such as traumatic brain injury but the fact that the lung calcification in our patient predated the brain injury by over 10 years makes it unlikely for the HO to have been due to the brain trauma. Other organ pathologies found at autopsy include chromophobe renal cell carcinoma, renal papillary necrosis, lymphocytic thyroiditis, and seborrheic keratosis.
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PMID:Idiopathic pulmonary calcification and ossification in an elderly woman with a missed diagnosis of subarachnoid haemorrhage. 2439 Dec 31

Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly prescribed for the treatment of pain, inflamation and fever. They are usually well tolerated in healthy persons, but in patients with risk factors (advanced age, renal impairment, heart failure, liver disease, concurrent medications with antihypertensive drugs), NSAIDs can induce serious renal adverse effects. They include sodium and water retention with edema, worsening of heart failure, hypertension, hyponatremia, hyperkalemia, acute kidney injury, chronic kidney disease, renal papillary necrosis and acute interstitial nephritis. The majority of these adverse effects are due to the inhibition of prostaglandins synthesis and they are dose and duration-dependent. Acute forms of kidney injuries are transient and often reversible upon drug withdrawal. Chronic use of NSAIDs in some patients may result in chronic kidney disease. It is recommended that patients at risk should have preventative strategies in place, including the use of the "lowest effective dose" of NSAID for the "shortest possible time" and monitoring renal function, fluid retention and electrolyte abnormalities. Patients who are taking antihypertensive medications should be monitored for high blood pressure and the doses of antihypertensive medications should be adjusted if needed. In general, the combination of NSAIDs and angiotensin inhibitors should be avoided. Some other preventive measures are dietary salt restriction, use of topical NSAIDs/non-pharmacological therapies and use of calcium channel blockers for treating hypertension.
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PMID:Prevention of Renal Complications Induced by Non- Steroidal Anti-Inflammatory Drugs. 2686 Oct 1


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