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Renal transplantation is associated with several abnormalities of function and structure of the musculoskeletal system. Some of these skeletal problems result from incomplete resolution of abnormalities of bone and mineral metabolism present at the time of transplantation. In this regard, persistent hyperparathyroidism, diabetes mellitus type 1, and accumulation of beta 2-microglobulin may lead to residual skeletal effects despite excellent function of the allograft. Persistent hyperparathyroidism may accelerate bone loss and increase the risk for osteonecrosis, as well as cause hypercalcemia and hypophosphatemia; some patients with severe hyperparathyroidism require parathyroid surgery. Osteonecrosis is the most debilitating skeletal complication after transplantation and frequently requires surgical therapy. Although osteomalacia associated with aluminum overload generally resolves after transplantation, bone complications due to dialysis amyloidosis and diabetes mellitus type 1 often fail to improve. Alternatively, skeletal abnormalities can be acquired after transplantation. Most of the new derangements of bone and mineral metabolism are due to the immunosuppressive medications. Toxic effects of glucocorticoids on bone contribute to the pathogenesis of osteonecrosis, increase the risk for fractures by decreasing cancellous bone mass and synthesis of bone matrix, and dampen the linear growth response in pediatric recipients. Whether cyclosporine independently causes appreciable toxic effects on bone metabolism is not yet clear, but use of this drug increases the prevalence of gout and dental problems. Osteonecrosis, osteopenia, and short stature remain important skeletal complications in recipients of renal allografts. Therapeutic efforts should be directed toward alleviating pretransplant bone disease and attenuating bone loss after transplantation.
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PMID:Musculoskeletal complications after renal transplantation: pathogenesis and treatment. 129 May 51

The islet amyloid polypeptide (IAPP) was originally identified by chemical analysis of the amyloid component in a human pancreatic islet cell tumor. It consists of 37 amino acids and displays about 50% homology with the neuropeptide calcitonin gene-related peptide (CGRP). In the pancreatic islets the IAPP is confined to the beta-cells, co-stored with insulin in the secretory granules and apparently co-secreted with insulin on glucose stimulation. In beta-cell depletion states such as streptozotocin diabetes in animals and in human type I diabetes mellitus both the IAPP and the insulin levels display reduction or are even absent. Within the mature IAPP molecule the amino acid sequence 23-29 shows considerable amino acid heterogenicity among various mammalian species. The amino acid composition of human IAPP in this specific region promotes the development of pancreatic islet amyloidosis, a phenomenon related to the ability to develop type II diabetes in that particular species. However, as type II diabetes is an inherited disease affecting a subpopulation of humans, not only the gene coding mature IAPP, but also one or several other hereditary factors of unknown origin are needed for the disease to develop. We have established a radioimmunoassay for plasma measurements of IAPP. During screening investigations of a large material of endocrine tumors we found a patient with extremely elevated plasma levels of IAPP, about 20,000 pmol/l. Immunohistochemical investigations confirmed the IAPP content and also revealed amyloid deposits. While performing an oral glucose tolerance test insulin levels remained unchanged whereas there was an increase in the glucose and IAPP levels. It is thus concluded that IAPP can be used as a tumor marker in pancreatic islet cell tumors and that high plasma levels of IAPP can inhibit glucose stimulated insulin secretion.
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PMID:Islet amyloid polypeptide (IAPP). A short review. 185 2

Gastrointestinal motility is the function of gastrointestinal smooth muscle. It is controlled by both the intrinsic and extrinsic nerves of the gastrointestinal tract and, to a lesser degree, the gastrointestinal hormones. Therefore, any abnormality of the above factors, theoretically, can cause gastrointestinal dysmotility. In a clinical situation, commonly seen is gastrointestinal dysmotility caused by either smooth muscle or intrinsic and extrinsic nerves dysfunction. Diseases that cause smooth muscle dysfunction include familial visceral myopathies, nonfamilial visceral myopathies, collagen disease, muscular dystrophies, amyloidosis, thyroid disease, and so on. Diseases that cause enteric nerve dysfunction include familial visceral neuropathies, nonfamilial visceral neuropathies, diabetes mellitus, Chagas' disease, ganglioneuromatosis of the intestine, visceral neuropathy of carcinomatosis, Parkinson's disease, and so on. The patients with neuromuscular disease of the gastrointestinal tract have a wide range of clinical manifestations regardless of the underlying cause. At one end of the spectrum, the patients may be asymptomatic, and at the other end of the spectrum, the patients may have functional obstruction of the gastrointestinal tract. Plain abdominal x-rays, upper gastrointestinal (UGI) and small bowel x-rays, enteroclysis, barium enema, and manometric studies are useful for the work-up of these patients. Enteroclysis is especially helpful in ruling out mechanical obstruction of the small intestine in patients with chronic intestinal pseudo-obstruction. Treatment is mainly symptomatic and supportive. There is no effective drug to improve gastrointestinal motility. Surgery may be helpful in selected cases of severe gastrointestinal dysmotility.
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PMID:Neuromuscular disease of the gastrointestinal tract. 200 Aug 94

Kidney biopsy (KB) is controversial in the elderly because it is generally felt that the risks exceed the potential therapeutic benefits. In this review of our personal experience and the literature reports, we discuss the risks of this diagnostic procedure and its use in the four main circumstances of patient referral. On the one hand, KB does not seem to be more hazardous in the elderly, provided that it is not performed in patients in poor condition or with atrophic kidneys or suspected vascular lesions. On the other hand, KB is clearly useful in a number of elderly patients either to assess the diagnosis of a systemic disease involving the kidney or to select the appropriate treatment. 1. In patients with non nephrotic proteinuria, KB should be performed if the proteinuria is associated with extra-renal signs suggestive of systemic disease or with deterioration of renal function. 2. Nephrotic syndrome without evidence of amyloidosis and diabetes, should lead to KB to identify patients with minimal change disease (MCD) requiring steroid treatment. Indeed, MCD can rarely be suspected on clinical grounds as the resulting nephrotic syndrome is rarely "pure" at this age. 3. In acute renal failure, KB seems to be essential and urgent in patients with rapidly progressive glomerulonephritis and in those with renal failure of dubious origin to select the most appropriate treatment according to the etiology and the type of renal lesions (sclerotic or "active"). 4. KB is useless and hazardous in chronic renal failure, except in case of unexplained rapid worsening of renal function in patients with previously moderate renal failure.
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PMID:[For or against renal biopsy after 65 years]. 209 Sep 64

Coexistent renal pathology with diabetic glomerulosclerosis was found in 38 of 136 (28%) consecutive renal biopsies performed primarily for proteinuria in individuals with diabetes mellitus. The histological lesions found were glomerulonephritis (14), focal tubulointerstitial disease (23), and amyloidosis (1). Significant microscopic haematuria was present in 66% of all patients and did not help to distinguish non-diabetic disease. The severity of diffuse diabetic glomerular disease was independently associated with duration of diabetes, raised plasma creatinine, the presence of hypertension, clinical retinopathy and neuropathy, but not with type of diabetes, degree of proteinuria or glycosylated haemoglobin at the time of biopsy. Diffuse interstitial fibrosis was related to the severity of glomerular disease and, if severe, also with a significantly (p less than 0.01) higher plasma creatinine. Coexisting renal disease was found to be associated with a significantly higher plasma creatinine (p less than 0.01) independent of the severity of diabetic glomerulopathy. Coexistent pathology is a not uncommon finding in renal biopsies from diabetic patients with proteinuria. These lesions and their underlying causes may not only influence the renal function and natural history of renal disease in diabetic individuals, but may also determine the response of proteinuria to therapy.
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PMID:A clinical-histological study of individuals with diabetes mellitus and proteinuria. 213 92

The degu, Octodon degus, is a South American hystricomorph rodent that is of interest because it develops spontaneous diabetes mellitus and has been found to have islet amyloidosis. To help clarify these problems we have cloned cDNAs encoding islet amyloid polypeptide (IAPP), insulin, and glucagon precursors from this species. The predicted amino acid sequence of degu IAPP is very similar to that of nonamyloid-forming guinea pig IAPP. In contrast, degu insulin and the C-terminal region of degu glucagon are highly divergent from those of other mammals, as is also the case in the guinea pig, suggesting the existence of some form of positive evolutionary pressure on these hormones of carbohydrate metabolism in the hystricomorph rodents.
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PMID:Cloning of complementary DNAs encoding islet amyloid polypeptide, insulin, and glucagon precursors from a New World rodent, the degu, Octodon degus. 229 24

We studied the clinical and pathological data for 334 patients age 65 or more who underwent renal biopsy for acute renal failure (ARF, n = 55), subacute renal failure (SRF, n = 72), chronic renal failure (CRF, n = 57), proteinuria (n = 137), and hematuria (n = 13). Tissue diagnoses were glomerulopathy (n = 252, 75.4%), acute tubular lesions (n = 18), interstitial nephritis (n = 23), vascular diseases (n = 36, including 14 with cholesterol emboli), and five miscellaneous diagnoses. Of the 55 patients with ARF, 23 had a glomerular lesion, 15 had acute tubular necrosis, and 8 had acute interstitial nephritis. Of 72 patients with SRF, 49 had a glomerulopathy, 12 had a vascular disorder, and six had acute interstitial nephritis. Hence, patients with ARF or SRF exhibited a high potential for reversible lesions. Only 11.3% of patients with CRF had potentially reversible causes. The most common causes of proteinuria were membranous glomerulopathy (34.3%), minimal change disease (14.6%), focal segmental sclerosis (11.7%), and amyloidosis (8.8%). Of the 25 patients with advanced nephrosclerosis, 24 had renal failure, 20 were hypertensive, and 13 had cholesterol emboli. Of 33 patients with diabetes mellitus, 66.7% were found to have lesions not related to diabetes. We conclude that renal biopsy is most useful in older patients with ARF or SRF because of potentially reversible renal disease. Old age alone is not a contraindication to performing a renal biopsy.
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PMID:Renal biopsy in patients 65 years of age or older. An analysis of the results of 334 biopsies. 235 29

The case of a 58-year-old man with nephrotic syndrome and characteristic pathologic renal lesions of KW disease is presented. No evidence of diabetes was found by oral or intravenous glucose tolerance tests. The possibilities of light-chain disease, membranoproliferative form of glomerulonephritis, and amyloidosis were excluded by histochemistry and immunofluorescent microscopy.
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PMID:Occurrence of intercapillary nodular glomerulosclerosis in the absence of glucose intolerance. 240 11

From 1982 to 1986, 1230 sudden death cases were autopsied in Osaka Medical Examiner's Office. Among them, 810 cases were sudden cardiac deaths (SCD) including coronary heart disease (77%), cardiomyopathy (7%), valvular disease (3%). All SCD cases were dead within 24 hours of the appearance of the fatal symptoms, and most of them (72%) were considered instantaneous death. Many of the fatal symptoms began in bed (31%), at bath (17%), at toilet (8%), or at work (8%). Thirty-four percent of them were thought by themselves or by their families to be healthy before the death. Hypertension (38%), coronary heart disease (13%) and diabetes mellitus (11%) were the major past history recorded. Microscopic observation of the hearts of 200 cases autopsied in 1986 showed various cardiac lesions: hypertrophy, atrophy, degenerations of myocytes, cellular and fatty infiltrations of the interstitium. According to their cardiac lesions and degrees of severity of coronary sclerosis, patients who died suddenly were divided into 8 groups as follows: 1. myocardial infarction (41) 2. myocarditis (6) 3. hypertrophic cardiomyopathy (19) 4. chronic ischemia with severe coronary sclerosis (65) 5. chronic ischemia with moderate coronary sclerosis (27) 6. small vessel disease (18) 7. amyloidosis (1) 8. unknown (23). These results suggest that coronary heart disease and hypertension play an important role in SCD.
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PMID:An epidemiologic and histopathological study of sudden cardiac death in Osaka Medical Examiner's Office. 263 29

We report a case of primary localized amyloidosis of the bladder which manifested post-renal failure. A 79-year-old woman with diabetes mellitus complained of anorexia and oliguria. Computed tomographic (CT) scan showed bilateral hydronephrosis. Cystoscopic examination revealed a broad-based nonpapillary tumor in the trigonum of the bladder and CT scan demonstrated thickening of the posterior wall of the bladder. Pathological examination of the transurethral biopsy specimen revealed amyloid deposits in the submucosa, but no malignant changes were found. Cytodiagnosis of washing fluid of the bladder revealed amyloid deposits around the exfoliative cells. Serum electrophoresis showed a normal pattern. Urinary Bence-Jones protein was not detected. Amyloid deposits were not found in rectal mucosa. Systemic or secondary amyloidosis was ruled out from these findings, and primary localized amyloidosis of the bladder was diagnosed. The mass of the bladder was transurethrally resected and pig-tail stents were indwelt. These procedures gave a satisfactory result.
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PMID:[A case of localized amyloidosis of the bladder manifesting post-renal failure]. 268 67


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