Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histomorphometry was performed on transiliac bone biopsies, double-labeled with tetracycline, from 60 consecutively admitted patients (20 women) at various stages of chronic renal failure (CRF). Eleven patients (1 woman) had normal bone resorption and formation indices. Bone resorption and osteoid formation increased with progression of renal failure, but abnormal values were seen even at slightly elevated creatinine levels. Mineralization lag time increased with CRF duration; prolonged values were only seen in patients with polycystic kidney disease or chronic pyelonephritis with advanced CRF. All patients with impaired mineralization also had increased bone resorption. Diabetes mellitus did not protect against skeletal lesions. The biochemical tests were too insensitive to predict type or severity of bone disease, and hand X-rays had no diagnostic value in early stages of renal osteodystrophy.
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PMID:Renal osteodystrophy in predialysis patients without stainable bone aluminum. A cross-sectional bone-histomorphometric study. 245 77

The case records of 327 patients who underwent bone biopsy in late or terminal renal failure, before any form of dialysis or transplantation, were examined for clues to the aetiology of renal osteomalacia and its manifestations. Fifty four per cent of the biopsies showed pure osteitis fibrosa, 34 per cent osteomalacia with osteitis fibrosa and 12 per cent showed neither abnormality. Osteomalacia was strongly associated with chronic pyelonephritis and obstructive uropathy as primary renal disease. In two matched groups of 100 each, and within the major primary diseases, it was associated with acidosis, hypocalcaemia and normophosphataemia (as opposed to hyperphosphataemia). There was no association with known length or uraemia and only a weak and inconsistent relationship with severity of uraemia. In the few patients studied, there was no relationship between osteomalacia and serum 25-hydroxycholecalciferol level. In contrast to the state of patients treated by haemodialysis, osteomalacia in this undialysed group was manifested by a higher level of serum alkaline phosphatase than pure osteitis fibrosa, serum iPTH did not differ between the groups, there was no predominance of symptoms in one group, other than proximal myopathy which had a weak association with osteomalacia, and Looser zones were more common than complete fractures. Our study shows that osteomalacia has different manifestations, and probably different causes, before and after the start of haemodialysis. These two stages of renal failure should be clearly distinguished in reports of renal bone disease.
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PMID:Osteomalacia in patients with chronic renal failure before dialysis or transplantation. 664 48

Between 1996 and 1997, 86 patients were treated for terminal renal failure by hemodialysis at Maribor Teaching Hospital. Among them were 12 with iPTH over 900 pg/ml and symptoms of bone disease. In these patients bone biopsy was carried out with the aim of determining the type of renal osteodystrophy (RO) and establishing a possible correlation with the clinical picture, with densitometry and laboratory results. Histomorphologically, 6 patients fulfilled the criteria for secondary hyperparathyroidism (HT) - 3 with analgetic nephropathy (AN), one with chronic pyelonephritis (CPN), one with vascular nephropathy (VN), one with chronic glomerulonephritis (CGN). Six patients fulfilled the criteria for mixed osteodystrophy (MO) - 3 AN, 2 CGN, one VN. According to laboratory findings and bone mineral density (BMD), a statistically significant difference between HT and MO was present only in AP (Table 1). The most frequent diagnosis in patients with iPTH >900 pg/ml was analgetic nephropathy.
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PMID:Patients with analgetic nephropathy on chronic hemodialysis have a high incidence of severe secondary hyperparathyroidism. 987 7

Primary hyperoxaluria type 1 (PH1) is caused by deficiency of peroxisomal alanine-glyoxylate aminotransferase which is in humans exclusively expressed in liver cells. The disease is inherited as an autosomal recessive trait, and initial symptoms usually occur in early childhood. Up to the age of 25 years, 90% of the patients are symptomatic, and many patients develop end-stage renal failure. Pronounced medical care is necessary in PH1 patients to prevent generalized oxalosis with complications due to bone disease and peripheral gangrene. The rather short survival of patients on hemodialysis is caused by sudden arrhythmias and heart block. As no dialysis procedure is able to remove the daily produced oxalate, early transplantation is mandatory. Our 45-year-old patient is remarkable on the basis of the late manifestations of PH1. The diagnosis was delayed by unspecific symptoms of nephrolithiasis with recurrent pyelonephritis. Clinical course and diagnostic cornerstones of primary hyperoxaluria are outlined. The principles of conservative treatment and experiences with dialysis and transplantation are discussed.
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PMID:Primary hyperoxaluria type 1 causing end-stage renal disease in a 45-year-old patient. 1117 30

Chronic kidney disease (CKD) is efined as a reduction in estimated glomerular filtration rate (eGFR) for three consecutive months, or evidence of kidney damage alone with preserved renal function. CKD affects 8.5% of the UK population. Early recognition allows intervention that may delay or avoid progression to end-stage disease and modify the cardiovascular risk associated with CKD. CKD is classified into five stages and the majority of individuals have stages 1-3, many of these will never progress to end-stage renal disease. A decline in with age is expected. The most frequent specific renal diseases resulting in progressive CKD in the UK are: diabetes mellitus, atheromatous renal vascular disease, glomerulonephritis, chronic pyelonephritis and inherited renal disease. Laboratories in the UK now routinely provide an eGFR with a serum creatinine value in all adult patients. This estimation is based on serum creatinine, age, gender, and ethnicity. Baseline assessment in a patient with newly diagnosed CKD should include: blood pressure, dipstick urinalysis, urine ACR or PCR, glucose, lipid profile and a full blood count. Fluctuation in renal function is common, particularly in elderly patients with CKD. A fall in eGFR can result from any intercurrent illness, medication, or volume depletion. Proteinuria is a very important prognostic marker in CKD, ACR is the preferred measure as it has greater sensitivity for lower levels of proteinuria and is the recommended method in those with diabetes. The potential health problems associated with CKD can be divided into two main categories: risk of progressive renal disease with the development of renal bone disease and renal anaemia, and risk of overt cardiovascular disease.
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PMID:Early recognition of CKD can delay progression. 2357 15

Hugh de Wardener died on 29th September 2013, ten days before his 98th birthday. He had a diverse upbringing and qualified in Medicine in 1939. He joined the army but was captured in 1942 and imprisoned in Singapore and Thailand until 1945. His clinical care of fellow prisoners was highly regarded. He preserved their clinical records and used them, post-war, to write two Lancet papers. One showed, for the first time, that Wernickes encephalopathy could be caused by severe malnutrition and cured by small doses of vitamin B1. His later academic interests were based on the emphasis he placed on renal physiology. This applied to the topic most associated with his name-Natriuretic Hormone. Whilst de Wardener never isolated this hormone, his early experiments, demonstrating that a third factor other than GFR and aldosterone affected renal sodium transport, were substantiated by others. Hugh had many research interests: pyelonephritis, renal histology, maintenance dialysis and metabolic/renal bone disease. In his later years he researched intensively into the role of sodium and salt in the aetiology of essential hypertension. Hugh was president of the International Society of Nephrology (1969-72) and the UK Renal Association (1975-78). He received many awards and recognitions from across the world, many of them after his (so-called) retirement. Throughout his career he never neglected the care of his patients. As Bob Schrier wrote in his obituary of de Wardener in Kidney International he was a caring physicianwhose dedication to his patients welfare was exemplary.
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PMID:Hugh de Wardener - the Man and the Scientist. 2691 74