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Query: UMLS:C0034186 (pyelonephritis)
 6,144 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The native kidneys in patients on dialysis or after transplantation tend to be overlooked until problems occur in relation to them. Their appearance can be variable and does not bear any consistent relationship to the cause of the renal failure; although in some cases, such as polycystic kidney disease, there are specific changes to be seen. Size can also be variable with little correlation to pathology in most cases. Acquired cystic disease of the kidneys is seen in up to 92% of long-term dialysis patients and also can be seen in patients with chronic renal failure. Proliferative changes occur in the kidneys which result in the development of cysts, adenomas and, in approximately 1% to 2% of dialysis patients, malignant lesions. It is probable that these changes are caused by a combination of factors, including circulating agents which are not cleared adequately by dialysis. There is some evidence that these changes are halted, or even reversed following a successful transplant. Problems with infection and hemorrhage may occur in patients with polycystic kidney disease. Problems with infection may also occur in patients with calculi, with longstanding pyelonephritis, or reflux.
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PMID:Ultrasonography of the native kidney in dialysis and transplant patients. 132 26

Pathogenic bacteria coexist with their hosts in a relationship which most frequently allows persistence of the bacteria without causing disease. In a small proportion of colonised individuals the complex mutual interaction between microbe and host is upset, leading to disease in the host. The investigation of bacterial virulence determinants and their genetic control at the molecular level is an important facet of the development of strategies to combat disease. This review focuses on the investigation of a single pathogenic organism as a means of illustrating modern approaches to the investigation of bacterial virulence. The importance of uropathogenic Escherichia coli in causing acute and recurrent pyelonephritis with the consequent morbidity of chronic renal failure is well established. Pyelonephritis-associated (Pap) pili are likely to be critical virulence factors in uropathogenic E. coli. The evidence for their role in pathogenicity and the control of their expression at the molecular genetic level is discussed.
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PMID:The molecular study of bacterial virulence: a review of current approaches, illustrated by the study of adhesion in uropathogenic Escherichia coli. 136 56

A 26 year old female, a case of chronic renal failure secondary to chronic pyelonephritis with renal osteomalacia, came with dimunition vision as the presenting complaint. She was found to have bilateral cataracts. All other known causes of cataract were excluded. Cataracts due to hypocalcaemia in chronic renal failure are a rare phenomenon.
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PMID:Bilateral cataracts as the presenting manifestation of chronic renal failure. 145 40

A 3-year-old boy with mixed glomerular/tubular proteinuria, mental retardation, and hyperkinesis is described. The proteinuria was discovered at the age of 3 years on urinary mass screening. Most of the urinary protein consisted of albumin, accompanied by increases in low molecular weight proteins, including beta 2-microglobulin and alpha 1-microglobulin. Mixed glomerular/tubular proteinuria is known to be caused by the following conditions: chronic renal failure, chronic pyelonephritis, cadmium poisoning, tubulointerstitial nephritis of various etiologies, and after strenuous, short-term, exhaustive exercise. The present patient did not display any of these disorders or conditions.
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PMID:Glomerular/tubular mixed-type proteinuria in a 3-year-old boy with mental retardation and hyperkinesis. 147 31

With the aim of determining the relative prevalence of the diseases underlying chronic renal failure (CRF) in a large homogeneous black tropical population, the autopsy records of the Obafemi Awolowo University Teaching Hospital over a four year period were studied. Out of a total of 702 cases coming to autopsy during this period, 66 (9.4%) died as a result of CRF. The highest number of cases of CRF fell within the 31-40 year age group with a male/female ratio of 1.28:1. Chronic glomerulonephritis was responsible for 40.9% of cases, malignant nephrosclerosis 16.6%, benign nephrosclerosis 7.6% while endstage renal disease (ESRD) was responsible for 15.4%. A miscellaneous group of diseases was responsible for 19.7%, about half of which was due to chronic pyelonephritis. Rarer causes of CRF were diabetic nephropathy, multiple myeloma, systemic lupus erythematosus and analgesic nephropathy.
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PMID:The pathological basis of chronic renal failure in Nigerians. An autopsy study. 149 21

We investigated the utility of measuring dysmorphic red blood cells (d-RBC) and urinary casts in the diagnosis and assessment of prognosis of renal diseases by evaluating these parameters in a total of 278 urine specimens from 78 patients with various renal diseases at our hospital. Urinary sediments obtained by the conventional method with in 4 hours after voiding were subjected to Sternheimer and Malbin's staining and examined under a conventional light microscope. We used the criteria we previously devised for classification of RBC as d-RBC and for classification of casts hyaline, granular, epithelial, red blood cell, white blood cell, fatty, or waxy. When there were 5 or more urinary sediment red blood cells per high-power field, d-RBC was found in 94% of samples from patients with chronic glomerulonephritis. The finding of d-RBC was not related to glomerulonephritis pathologically diagnosed according to the WHO classification system for biopsy specimens. Even when there were fewer than 5 red blood cells per high-power field, d-RBC was sometimes found. Casts of all types were found in samples from patients with chronic glomerulonephritis or chronic renal failure. In samples from patients with chronic pyelonephritis, however, white blood cell, fatty, and waxy casts were not found, and less than 1 granular or epithelial cast per low-power field was found. The findings for the presence and the extent of both d-RBC and casts were in good accord with and changed with the clinical course, indicating that d-RBC and casts of urinary sediment can be used to predict the prognosis of patients with renal disease.
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PMID:[Clinical significance of urinary sediment dysmorphic red blood cells and casts in renal disease]. 150 90

The term "renal osteodystrophy" is used to include skeletal disorders of patients with chronic renal failure: osteitis fibrosa, osteomalacia, osteosclerosis, osteoporosis and the frequently associated extraskeletal calcifications. It is the chronic glomerular disease with phosphate retention and resultant hyperphosphatemia on one hand and deficient 1,25 (OH)2 D3 and resultant hypocalcemia on the other to induce secondary hyperparathyroidism. The three most common causes of chronic renal failure in our patients are chronic glomerulonephritis, diabetic nephropathy, hypertensive nephropathy in decreasing frequency, polycystic renal disease occurs in five patients. Other miscellaneous causes include nephrotic syndrome, chronic pyelonephritis, systemic lupus erythematosus, periarteritis nodosa, interstitial nephritis and renal stones. The bone changes are similar in primary and secondary hyperparathyroidism and the incidence of brown tumor is about 3% in the former and 1.5 to 1.7% in the latter. We present one among the 94 dialyzed patients who has long-standing severe chronic renal failure from polycystic kidney disease and develops brown tumor in the mid ulna after 7 years on maintenance hemodialysis. The incidence of brown tumor in our series is about 1.1%. Because of increased longevity of the dialyzed patients, brown tumor from secondary hyperparathyroidism is now more commonly observed. Hyperphosphatemia with serum calcium-phosphate products exceeding plasma solubility of 60 to 75 mg/dl may induce soft tissue and vascular calcification. This explains the much higher incidence of soft tissue calcification in secondary than primary hyperparathyroidism; two of our patients with generalized Monckeberg's type arterial calcification and multiple periarticular calcifications in five patients have been observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal osteodystrophy. 164 77

We have treated 167 patients with staghorn calculi. Conservative therapy was used in 61 patients who have been followed up for 1 to 18 years (average 7.8). Chronic renal failure occurred in 22 of these patients and 7 died from uraemia. The causes of chronic renal failure were bilateral staghorn calculi, staghorn calculi and contralateral urinary calculi, and chronic pyelonephritis of the contralateral kidney. The morbidity and mortality rates following conservative treatment were higher than those following surgical management. The pathological findings in 47 kidneys after nephrectomy showed severe hydronephrosis, renal abscess and xanthogranulomatous pyelonephritis. These results indicated that staghorn calculi destroyed the kidney and early complete removal of these stones is advisable.
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PMID:Staghorn calculi--long-term results of management. 188 36

The authors used monoclonal antibodies to human transferrin for the development of a high-sensitive test system for the assessment of transferrin levels in urine with enzyme immunoassay. The conditions of the immunoassay performance were optimized. The sensitivity of the test system enabled the authors to define the levels of transferrin up to 1 ng/ml. Tests for the detection of transferrin in patients with chronic pyelonephritis and chronic renal failure were performed. The designed test system permitted transferrin to be revealed in the urine of those patients who had negative results during a radial immunodiffusion. The authors demonstrated the possibility of using the developed monoclonal antibodies in laser nephelometry for the detection of blood and urinary transferrin levels.
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PMID:[The use of monoclonal antibodies for determining the transferrin content of the urine]. 197 11

Investigation of renal biopsy specimens from 488 patients with diabetic glomerulosclerosis (DGS) of varying severity revealed the following: 1) The severity of DGS increases with the duration of the diabetes. 2) As the severity of DGS increases, it is complicated with increasing frequency by exudative changes, which correspond in detail to hyperperfusion lesions described in the literature. 3) As the severity of DGS increases, the severity of arteriolosclerosis and the incidence of nephrotic syndrome increase significantly. 4) The 5- and 10-year renal survival rates are highest for those diabetic patients in whom the tubules and renal cortical interstitium are of normal appearance. These survival rates are diminished if any of the following are present at the time of biopsy: a) interstitial fibrosis; b) hyperperfusion lesions; c) nephrotic syndrome; d) elevation of the serum creatinine concentration to more than 1.3 mg%. 5) No significant correlation was found between renal survival rate and age, sex, or type of diabetes. 6) The inflammation of the renal interstitium seen in diabetes does not differ from that seen in chronic glomerulonephritis. Monocytes, macrophages, T lymphocytes, fibroblasts and fibrocytes play the major role in this inflammation. This inflammatory process is considered to represent not pyelonephritis, but rather an auto-immune process. In other words, it is proposed that the diabetic kidney fails not only as a result of non-specific glomerular lesions (hyperperfusion lesions) but also because of non-specific tubulointerstitial changes, whereas diabetic glomerulosclerosis alone does not lead to chronic renal failure.
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PMID:The pathogenesis of chronic renal failure in diabetic nephropathy. Investigation of 488 cases of diabetic glomerulosclerosis. 206 8


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