Cases reported "Kidney Failure, Chronic"

Filter by keywords:



Filtering documents. Please wait...

1/23. Severe hyperparathyroidism with hypercalcemia associated with chronic renal failure at pre-dialysis stage.

    We report a case of a 23-year-old Japanese woman who had severe hyperparathyroidism associated with chronic renal failure before the start of dialysis treatment. Her chief complaints were swelling and pain in both shoulders. Laboratory examination revealed renal failure (BUN 134 mg/dl, serum Cr 7.3 mg/dl), severe normocytic normochromic anemia (hemoglobin 4.3 g/dl), hypercalcemia (11.8 mg/dl), and hyperphosphatemia (9.7 mg/dl). serum PTH levels were extremely increased (intact PTH >1,000 pg/ml: normal range 10-50 pg/ml). X-ray examination of the skull and shoulders showed a salt and pepper appearance, and cauliflower-like deformity of the distal end of both clavicles, respectively. Accelerated ectopic calcification was observed in the costal cartilages, internal carotid arteries, and splenic arteries. Ultrasonographic examination revealed enlargement of the four parathyroid glands. thallium-technetium subtraction scintigraphy of the parathyroid glands showed increased uptake into the upper two. Renal needle biopsy revealed severe impairment of the interstitium and tubules with much milder changes in glomeruli. The etiology of the renal failure could not be identified. Hemodialysis, total parathyroidectomy and auto-transplantation into the forearm were immediately performed. The pathological diagnosis was chief cell hyperplasia of the parathyroid glands. Based on the presence of chronic renal failure, remarkable hyperphosphatemia with mild hypercalcemia, an unusually high level of serum PTH, and accelerated ectopic calcification, the patient was diagnosed to have severe secondary hyperparathyroidism caused by chronic renal failure with major impairment of the renal interstitium and tubules.
- - - - - - - - - -
ranking = 1
keywords = tubule
(Clic here for more details about this article)

2/23. azoospermia due to testicular amyloidosis in a patient with familial mediterranean fever.

    We describe a patient suffering from familial mediterranean fever (FMF) who presented to our clinic with secondary infertility of 2 years due to amyloid A amyloidosis. His spermiogram disclosed azoospermia. A testicular biopsy revealed hyalinized tubules devoid of full spermatogenesis and containing abundant amyloid, confirmed by congo red stain. We suggest that testicular amyloidosis be taken into consideration when dealing with azoospermic FMF patients. In view of the progressive nature of amyloid accumulation in the testis we propose to follow routinely the spermiogram of FMF patients with renal amyloidosis. Furthermore, consideration of sperm cryopreservation is suggested in these cases. In FMF patients with azoospermia consideration of testicular biopsy is recommended as early as possible in order to increase the chance of sperm retrieval.
- - - - - - - - - -
ranking = 0.5
keywords = tubule
(Clic here for more details about this article)

3/23. An autopsy case of mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes syndrome with chronic renal failure.

    A 25-year-old man developed a stroke-like episode. He suffered from renal failure and became dialysis-dependent. His mother was also dialysis-dependent. A3243G point mutation of the mitochondrial tRNA(leu) gene was detected in both of them. The patient was diagnosed with mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS), and died of a recurrence of stroke-like episodes at the age of 30. autopsy revealed numerous abnormal mitochondria in the kidneys, but no renal vascular changes. This is the first report of a MELAS case in which the presence of numerous abnormal mitochondria in podocytes and tubules was confirmed by electron microscopy.
- - - - - - - - - -
ranking = 0.5
keywords = tubule
(Clic here for more details about this article)

4/23. Dysplasia of tubular cells in a kidney- transplanted patient treated with recombinant human growth hormone.

    After renal transplantation (Tx), children with growth retardation can be successfully treated with recombinant human growth hormone (rhGH). However, the impact of this treatment on kidney allograft function remains a source of concern. We report on one boy who received a cadaveric kidney transplant at 12 yr of age, after developing end-stage focal and segmental glomerulosclerosis and hyalinosis. The early post-transplant period was complicated by thrombosis of an arterial branch of the graft and two acute rejection episodes. Because of poor growth, the boy was treated with rhGH starting 22 months after the Tx. The renal function remained relatively stable for 22 months after initiation of rhGH therapy and then progressively deteriorated over a period of 10 months, with the patient ending up on dialysis. Several biopsies, performed for rejection episodes or before the start of rhGH, or to elucidate the deterioration of the renal function, were analyzed. Histologically, a progressive increase in the amount of hypertrophy of the tubules and of the glomeruli was seen after initiation of rhGH. hyperplasia of the tubular epithelium with crowding of cells of the proximal tubules, hyperchromasia and irregularities in the shape of the nuclei, and abrupt changes of chromatism along the tubuli, were also observed. These lesions of tubular dysplasia are extremely unusual in transplanted kidneys and are unlikely to be caused by compensatory hypertrophy secondary to destruction of renal tissue. They may be an effect of rhGH treatment. The prognostic significance of these lesions is unknown but merits attention.
- - - - - - - - - -
ranking = 1
keywords = tubule
(Clic here for more details about this article)

5/23. Zonal distribution of glomerular collapse in renal allografts: possible role of vascular changes.

    Collapsing glomerulopathy (CG), an aggressive variant of focal segmental glomerular sclerosis, is a renal disease with severe proteinuria and rapidly progressive renal failure. The pathogenesis of CG is unknown. It strongly resembles human immunodeficiency virus (hiv)-associated nephropathy, but the patients are hiv negative. The characteristic glomerular lesion is capillary loop collapse with prominent podocytes filling Bowman's space. Interestingly, these glomerular changes are usually associated with severe tubulointerstitial injury, including tubular epithelial degenerative changes, microcystic dilation of several tubules, and interstitial inflammatory cell infiltrate. Recently, it became evident that the morphologic pattern of CG may appear not only in native kidneys, but also de novo in renal allografts, and that the pattern of CG in renal transplants is not always associated with severe proteinuria. Studies describing CG in renal allografts are all based on biopsies. We report 3 allograft nephrectomy specimens that showed a zonal distribution of the characteristic collapsing glomerular changes with associated tubulointerstitial injury. All 3 kidneys had obliterative vascular changes. One nephrectomy specimen had chronic obliterative transplant arteriopathy, 1 had acute vascular rejection, and 1 had thrombotic microangiopathy. None of the patients had severe proteinuria. Our cases suggest that the morphologic pattern of CG in renal allografts may not represent the same disease process as CG in native kidneys and provide further evidence that collapsing glomerular changes do not define the disease entity of CG, but rather represent a pattern of renal injury. Among other factors, hemodynamic disturbance may play a role in the development of the pattern of CG in renal allografts.
- - - - - - - - - -
ranking = 0.5
keywords = tubule
(Clic here for more details about this article)

6/23. nephrogenic fibrosing dermopathy with systemic involvement.

    BACKGROUND: There is a growing literature regarding sclerotic and panniculitic cutaneous conditions seen in patients with end-stage renal disease (eg, calciphylaxis and soft tissue calcification). nephrogenic fibrosing dermopathy (NFD) is a recent designation to describe cutaneous findings in patients with end-stage renal disease who developed sclerotic plaques with scleromyxedema-like histologic features. Soft tissue calcification is rare in patients with NFD and systemic involvement has not been reported. OBSERVATIONS: We describe a patient with end-stage renal disease who developed diffuse indurated woody plaques consistent with NFD in association with soft tissue calcification with catastrophic sequelae. A deep excisional biopsy specimen from the patient revealed thickened collagen bundles in the reticular dermis, plump bipolar spindle cells, and increased mucin. Focally, there were zones of calcium deposition in dermal collagen without vessel calcification. autopsy of the patient revealed extensive fibrosis and calcification of the diaphragm, psoas muscle, renal tubules, and rete testes. The patient died 11 months after developing NFD. CONCLUSION: A subset of patients with NFD may have significant systemic involvement.
- - - - - - - - - -
ranking = 0.5
keywords = tubule
(Clic here for more details about this article)

7/23. Rational diuretic management in congestive heart failure: a case-based review.

    The pharmacology and pharmacokinetics of diuretics are unique among therapeutic drugs. knowledge of these principles can be used to great advantage in the management of heart failure, whereas ignoring them can lead to either minor or life-threatening adverse consequences. Two major categories of potential therapeutic problems are diuretic resistance and the development of disturbances in serum potassium and other electrolytes. Inhibition of sodium reabsorption in the loop of henle or distal convoluted tubule leads to renal potassium wasting, whereas inhibition of sodium reabsorption in the collecting duct (either directly, as with triamterene or amiloride, or through aldosterone antagonism) causes potassium retention. Combining diuretics of different classes, a rational and frequently used strategy to counter diuretic resistance, can be anticipated to balance or magnify these effects, depending on the site of action of the individual drugs.
- - - - - - - - - -
ranking = 0.5
keywords = tubule
(Clic here for more details about this article)

8/23. Renal cell therapy in the treatment of patients with acute and chronic renal failure.

    Hemodialysis and hemofiltration have been important technologies in saving the lives of patients with acute (ARF) and chronic renal failure by clearing small solutes from plasma and thereby preventing death from acidemia, hyperkalemia, volume overload, and uremia. These therapeutic approaches, however, are still suboptimal, as patients with ARF have mortality rates exceeding 50%, and patients with end-stage renal disease (ESRD) have, on average, a life expectancy of 4-5 years. The preeminent cause of death in patients with ARF is the development of sepsis or the systemic inflammatory response syndrome with resulting systemic vasodilation, hypotension, ischemic injury to solid organs, multi-organ failure, and death. This vasodilation is due to persistent and excessive pro-inflammation. Similarly, the reduced survival times of patients with ESRD on chronic dialysis have been associated with a persistent and chronic systemic pro-inflammatory state. We have hypothesized that the loss of renal tubule cell mass acutely in acute tubule necrosis and chronically in ESRD results in an immunologically dysregulated state leading to excessive pro-inflammation. The replacement of renal tubule cell function may thus change the current dismal prognosis of patients with these disorders. In this regard, this report presents the first patient ever treated with a bioartificial kidney consisting of a synthetic hemofilter in series with a renal tubule assist device (RAD) containing approximately 10(9) human renal tubule cells. This treatment in a critically ill patient with multi-organ failure and ARF in the intensive care unit was associated temporally with improved cardiovascular parameters and enhanced native kidney function. Multiple systemic plasma cytokine levels and gene expression profiles of peripheral white blood cells were also temporally changed with cell therapy. Clinical trials in patients suffering from either ARF or ESRD are currently ongoing to evaluate the influence of the RAD on the inflammatory response in these groups of patients.
- - - - - - - - - -
ranking = 2.5
keywords = tubule
(Clic here for more details about this article)

9/23. alkaptonuria and renal failure: a case report and review of the literature.

    In alkaptonuric ochronosis, the absence of homogentisic acid oxidase results in the accumulation of homogentisic acid in the body. Associated renal failure is rare and usually occurs in the later stages of the disease. We report a 19-yr-old girl who presented initially with severe renal failure, without family or past history of illness. There was no significant proteinuria or hematuria. No clinical evidence of pigmentation such as skin and subcutaneous cartilages was noted. However, pigment deposits were identified in the renal biopsy specimens obtained within a week after admission and another after a month. Two months later the peritoneal dialysis fluid and skin progressively darkened, suggesting ochronosis. This was confirmed by the detection of homogentisic acid in the serum and urine. The patient expired in renal failure. Renal biopsy tissues showed diffuse chronic tubulo-interstitial disease characterized by widespread tubular atrophy, interstitial fibrosis, and a moderate degree of inflammation. Many tubular cells contained brown, coarsely granular ochronotic pigment (OP) and a few pigment casts were in the lumina. Similar deposits were also in the interstitium and within histiocytes. Ultrastructural studies of the glomeruli revealed small sparse OP deposits in the visceral and parietal epithelial cells, mesangial cells, and rare extracellular and basement membrane deposits. The tubulointerstitial changes were varied: atrophy and dilatation of tubules, varying degrees of lysosomal OP and degeneration of tubular cells, casts containing OP with crystalline material, histiocytes distended with OP, and free interstitial pigment deposition.(ABSTRACT TRUNCATED AT 250 WORDS)
- - - - - - - - - -
ranking = 0.5
keywords = tubule
(Clic here for more details about this article)

10/23. Fanconi's syndrome induced by a monoclonal Vkappa3 light chain in Waldenstrom's macroglobulinemia.

    Fanconi's syndrome (FS) is a disorder of sodium-dependent proximal tubule reabsorption, which may complicate plasma cell disorders producing a free monoclonal light chain (LC). FS often occurs in the setting of smoldering myeloma and features cytoplasmic crystalline inclusions of monoclonal kappa LC in proximal tubular cells and malignant plasma cells. Although the clinical and pathological presentation may vary, including lack of crystal formation, monoclonal kappa LCs that underlie FS show a striking genetic and biochemical homogeneity: they almost always belong to the Vkappa1 subgroup of variability and originate from 2 germline genes, O2/O12 or O8/O18. Their variable domain sequences present unusual hydrophobic residues, responsible for the resistance to proteolysis, which leads to LC accumulation in the endocytic compartment of proximal tubule cells. We report a patient with slowly progressive Waldenstrom's macroglobulinemia and full-blown FS with accumulation of a monoclonal kappa LC within proximal tubules, but no detectable crystalline organization. This LC, which belonged to the unusual Vkappa3 subgroup and derived from the L2/L16 germline gene, showed no common substitution with previously described FS kappaI LC and was sensitive to trypsin digestion. These data show that molecular and biochemical characteristics of kappa LCs in patients with FS are more heterogeneous than initially suspected. Mechanisms other than resistance of LCs to endosomal proteolysis probably are involved in the pathogenesis of FS-associated plasma cell dyscrasias.
- - - - - - - - - -
ranking = 1.5
keywords = tubule
(Clic here for more details about this article)
| Next ->


Leave a message about 'Kidney Failure, Chronic'


We do not evaluate or guarantee the accuracy of any content in this site. Click here for the full disclaimer.