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

The renal acidosis may appear by a decrease of the number of nephrons able to function (decrease of the filtrate of the glomerulum) as well as by a selective alteration of the tubular acidification mechanism. In 66 patients with chronic renal insufficiency of different degrees of severity (32 patients with diabetic glomerulosclerosis, 18 patients with chronic glomerulonephritis and 16 patients with chronic pyelonephritis) studies of the parameters of the acid-base-state and the renal insufficiency were carried out. 53 of these patients had a pathologically changed acid-base-state which was most expressed in patients with chronic pyelonephritis. A characteristic relation between the renal function (creatinine clearance) and the change of the pH-values was observed. The regression curve of the pH-values was descending so that in clearance values below 25 ml/min in nearly all patients a pronounced acidosis was present. This could be proved in the patients with pyelonephritis already when higher clearance values were present. The forms of the development of the metabolic acidosis in chronic renal insufficiency are discussed.
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PMID:[Metabolic acidosis in chronic renal insufficiency of various etiology]. 2 13

Renal complications occur frequently in diabetics. Glomerular lesions exist in basal membrane thickening, diffuse and nodular glomerulosclerosis, exudative lesions and glomerular aneurysms. Tubular and interstitial changes are characterized by Armanni-Ebstein cells, by pyelonephritis and papillary necroses. Vascular changes occur in the form of arteriosclerosis and arteriolosclerosis. Nodular glomerulosclerosis is characteristic of diabetic renal damage, all other changes only occur more frequently in diabetics. Recently, studies deserve attention which suggest a regression of glomerular lesions if the diabetic metabolism is normalized.
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PMID:[Morphology of diabetic nephropathy (author's transl)]. 40 64

Follow up studies in 19 diabetic patients with manifestation in the youth. Proteinurie within few years; later on nephropathy: 7 cases with glomerulosclerosis, 8 with arteriolosclerosis, 3 with pyelonephritis and 1 with chronic glomerulonephritis. In all cases retinopathy, very often coronarsclerosis, seldom peripheral and cerebral sclerosis. 14 patients died, mostly in young age in consequence of nephropathy. Proteinurie is a malignant symptom of diabetic angiopathy; in contrast to the retinopathy.
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PMID:[Diabetic angiopathy. Proteinuria as an initial symptom]. 54 May 65

The term diabetic nephropathy includes the Kimmelstiel-Wilson intercapillary glumerulosclerosis (1936), arterio-arteriolosclerotic changes and pyelonephritis. In principle, diabetic nephropathy becomes more frequent with increasing duration of diabetes mellituus. Pyelonephritis is 4 to 5 times more frequent in diabetics than in the general population. Elderly overweight women are particularly at risk. - Only the nodular intercapillary glomerulosclerosis and not the diffuse or exudative form is specific for diabetes mellitus. It is found in 20-40% of all diabetics who have had the disease for 10-15 years. Whether the microangiopathy is typical of diabetes mellitus remains to be seen. Due to the intense cardiovascular changes, possible disorders of brain and liver function and infection, the prognosis of renal insufficiency is considerably worse in diabetics than in non-diabetics.
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PMID:[Diabetic nephropathy (author's transl)]. 81 41

The diagnosis of arteriosclerosis is simple. The chronic pyelonephritis, however, is in most cases not clearly to be diagnosed, but only with a certain probability. To the glomerulosclerosis is applied that conspicuous findings allow of a doubtless diagnosis. But not in the least seldom there exist certain difficulties, above all in the initial stage and in the clear limitation to glomerulonephritis. In the majority of these cases the modern morphologic investigation methods lead to a clarification, but also the exact anamnestic and clinical data may be very useful for a probability diagnosis.
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PMID:[Kidney biopsy in the differential diagnostic clarification of renal diseases in diabetic patients]. 119 61

With the purpose of establishing the clinicopathologic correlation in pyelonephritis and to discard other interstitial nephrites, with present day morphologic criteria we analysed 63 casos that had been diagnosed as pyelonephritis, following Weiss and Parker's histologic criterion. The clinicopathologic diagnosis of pyelonephritis was confirmed in 12 cases; all of them showed obstructive uropathy and in most of them, there was chronic renal failure. Interstitial nephritis was established in 27 cases, all of them showing septicemia and almost half of the cases showed acute renal failure. Other 20 cases showed tubulointerstitial nephritis secondary to different types of glomerulopathies, fetal glomerulosclerosis, dysplasias, nephrophthisis, radiation nephritis and renal infarct. In 4 cases, the study of sections finer than the original, showed absence of histopathologic lesions. The results of the present study point out the main causes of confusion with the pathological diagnosis of pyelonephritis, the necessity to investigate predisposing uropathy in patients with urinary infection and stresses the importance to establish correlation with clinical and laboratory findings in cases with tubulointerstitial lesions.
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PMID:[Pyelonephritis and bacterial tubulointerstitial nephritis]. 125 17

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

Chronic pyelonephritis (c.p.) is by definition an infectious tubulo-interstitial nephritis. It has to be differentiated from other etiologic forms of tubulo-interstitial nephritis. Therefore strict morphological criteria are needed for diagnosis. The characteristic lesion is a large cortico-medullary scar overlying a dilated chronically inflammed calyx. The macroscopic aspect and the histologic survey picture are more important than histologic details. A diagnosis on renal biopsies is therefore not warranted. Vesico-renal reflux and papillary morphology play an important pathogenetic role. Beside the more common focal scar a diffuse form of scarring can be observed. A limited number of conditions only have to be considered in differential diagnosis. The Ask-Upmark kidney seems to be a special form of c.p. related to urinary tract infection and reflux in early infancy. Pelvi-calyceal lithiasis without superimposed infection causes a picture very similar to a pyelonephritic scar. A reliable differentiation between c.p. and analgesic nephropathy may cause problems in endstage kidneys with sloughed off papillae. Various mechanisms of renal damage such as bacterial infection, immunological mediated inflammation, leakage of urinary constituents into the interstitium especially Tamm-Horsfall-protein and ischemia have to be considered. Despite the frequency of urinary tract infections chronic progressive pyelonephritis is rare. Predisposing factors are needed for progression of the disease. These include congenital or acquired urinary tract obstruction, vesico-renal reflux and papillary damage with intrarenal obstruction to the urinary flow. Other important factors are focal and segmental glomerulosclerosis and hypertension.
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PMID:[Chronic pyelonephritis and its differential diagnosis. A disease changing with time]. 248 12

We report a case of xanthogranulomatous pyelonephritis in a cadaver kidney allograft. The patient had diabetic glomerulosclerosis. The predisposing factors that led to this condition included hyperglycemia, a previous rejection reaction and Escherichia coli urinary infection. Persistent fever, pyuria, bacilluria and a nonfunctioning allograft resulted in allograft nephrectomy. The diagnosis was made on histological examination. Diagnostic criteria for xanthogranulomatous pyelonephritis in the allografted kidney are similar to those in the native kidney.
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PMID:Xanthogranulomatous pyelonephritis in a renal allograft. 305 33

Using standard real time sonography, renal cortical echogenicity, renal length, intrarenal cystic structures and renal calculi were evaluated in 63 patients (30 men, 33 women) in end-stage renal parenchymal diseases (glomerulonephritis n = 21, diabetic glomerulosclerosis n = 9, analgesic nephropathy n = 14, chronic atrophic pyelonephritis n = 19). Patients with glomerulonephritis and diabetic glomerulosclerosis presented with larger kidneys and only slightly increased cortical echogenicity as compared to analgesic nephropathy and chronic atrophic pyelonephritis. In addition, intrarenal cystic structures were found in 50% of the patients with analgesic nephropathy and in 31% of the patients with pyelonephritis, compared with only 14% and 11% in patients with glomerulonephritis and diabetic glomerulosclerosis, respectively. Intrarenal calcifications were more frequent in pyelonephritis and analgesic nephropathy. In end-stage renal parenchymal disease, sonography might be able to distinguish between different types of renal medical disorders.
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PMID:[Ultrasound in terminal renal failure--etiologic conclusions?]. 307 Jul 47


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