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Kidney biopsies

Minor surgery within past 10 days, including liver and kidney biopsy, thoracocentesis, lumbar puncture ... [Pg.72]

Kidney biopsy (collection of a tissue sample of the kidney for the purpose of microscopic evaluation may aid in the diagnosis of glomerular and interstitial diseases)... [Pg.364]

It is often difficult to differentiate ARF from acute rejection in the kidney transplant recipient, as both conditions may present with similar symptoms and physical examination findings. However, fever and graft tenderness are more likely to occur with rejection while neurotoxicity is more likely to occur with cyclosporine or tacrolimus toxicity. Kidney biopsy is often needed to confirm the diagnosis of rejection.42... [Pg.371]

Other markers for structural kidney damage that can be used in place of proteinuria include abnormalities in urinary sediment, such as hematuria, or abnormalities in imaging studies or kidney biopsy.1... [Pg.377]

A 62-year old woman was admitted to hospital with lupus nephritis. A kidney biopsy showed a mesangio-proliferative glomerulonephritis (WHO class III). After 4 months of inadequate response to traditional... [Pg.33]

Fig. 4. Kidney biopsy. The findings suggested acute tubular necrosis (p. 4)... Fig. 4. Kidney biopsy. The findings suggested acute tubular necrosis (p. 4)...
Serum myoglobin (ng/ml) CPK (U/l) Myoglobinuria Kidney biopsy Hypouricemia... [Pg.34]

In 5 of the 22 patients, a kidney biopsy was performed. The findings suggested that these patients were in the recovery phase of acute tubular necrosis. [Pg.50]

In 54 patients, a kidney biopsy was performed 13.2 8.9 days after onset (n = 32). In all patients, the findings suggested either acute tubular necrosis or its recovery phase. The underlying diseases included kidney diseases such as IgA nephropathy [138], minimal change nephrotic syndrome [139], autosomal dominant polycystic kidney disease (ADPKD) [140], and cystinuria [67]. [Pg.55]

On June 6, this patient developed severe loin pain after he participated in two 150-m sprints at a town athletics meeting. After 5 days, he was referred to the outpatient clinic of our department. His serum creatinine and uric acid levels and FEUA, were 2.9mg/dl, 2.1 mg/dl, and 49.7%, respectively. His creatine phosphokinase (CPK) level was normal. When his serum creatinine level decreased to 1.58 mg/dl, a contrast medium was administered. A delayed computed tomography (CT) scan after 24 and 48 h confirmed patchy wedge-shaped contrast enhancement (Fig. 58). Under a diagnosis of ALPE, his body water balance (hydration) was controlled. In this patient, recovery was achieved 4 weeks after onset, and his serum creatinine and uric acid levels were then 1.0 mg/dl and 0.6 mg/dl, respectively. Furthermore, load tests with a uric acid reabsorption inhibitor (benzbromarone) and a uric acid excretion inhibitor (pyrazinamide) suggested presecretory reabsorption defect-related renal hypouricemia. A kidney biopsy 16 days after onset confirmed the recovery from acute tubular necrosis. [Pg.65]

Mihatsch MJ, Antonovych T, Bohman SO, Habib R, Helmchen U, Noel LH, Olsen S, Sibley RK, Kemeny E, Feutren G. Cyclosporin A nephropathy standardization of the evaluation of kidney biopsies. Clin Nephrol 1994 41(l) 23-32. [Pg.765]

Feutren G, Mihatsch MJ. Risk factors for cyclosporine-induced nephropathy in patients with autoimmune diseases. International Kidney Biopsy Registry of Cyclosporine in Autoimmune Diseases. N Engl J Med 1992 326(25) 1654-60. [Pg.765]

One renal transplant recipient developed the nephrotic syndrome, with microscopic hematuria and non-ohguric acute renal insufficiency within 15 days after starting foscarnet therapy for cytomegalovirus infection (13). A kidney biopsy showed crystals in aU glomeruh and in the proximal tubules. The crystals consisted of several forms of foscarnet salts. Renal function and proteinuria nevertheless improved progressively, and a second transplant biopsy 8 months after the first one showed... [Pg.1447]

Drug-specific T cells have been identified in the blood of patients and persist for months after the adverse reaction [74]. Drug-specific T-cell clones have been derived they produce IL-4, IL-5, TNF-a and inconstantly IFN-y. The similarity between the TCRVp expressed by drug-specific T-cells in the blood and those expressed by T-ceUs in the kidney biopsies strongly suggest that drug-specific T cells localize into the kidneys [74] and orchestrate inflammation. [Pg.138]

Acute tubular necrosis, tubulointerstitial nephritis, and glomerulonephritis have been described in patients with foscarnet-induced acute kidney injury [54, 59-62]. Kidney biopsy specimens from patients who had received foscarnet have, in several reports, shown the presence of crystals within glomerular capillaries... [Pg.386]

Medications in this class include delavirdine, efa-virenz, and nevirapine. Similar to the NRTls, these agents bind to viral reverse transcriptase and block DNA polymerase activity. A key difference is that NNRTIs do not require intracellular phosphorylation and are not incorporated into viral DNA. Clinically significant kidney toxicities or specific fluid-electrolyte complications have not been reported with this class of agents. In the rat model, efavirenz was associated wifh a species specific dependent kidney toxicity which occurred secondary to the development of a unique glutathione conjugate produced as a metabolite of efavirenz associated with renal tubular epifhelial cell necrosis [125-126]. This toxicity has not been observed in humans. One patient was recently reported to have reversible nephrotic-range proteinuria attributed to efavirenz use, in which a kidney biopsy showed diffuse podocyte foot process effacement [127]. Another report noted the development of rhabdomyolysis and acute tubular necrosis as a result of a drug interaction between delavirdine and atorvastatin [128]. Kidney toxicity due to nevirapine has not been reported. [Pg.389]

Interstitial nephritis has been found in kidney biopsies in patients treated with indinavir [146-151]. Some of these cases have described eosinophiluria and crystals (assumed to be indinavir) associated with histiocytes and giant cells in the renal tubules. Some of these patients were asymptomatic, while others reported classic symptoms of nephrohthiasis. Cortical atrophy was found in some patients, suggesting the progression from acute injury towards chronic kidney disease [152]. [Pg.391]

Other protease inhibitors have also been rarely associated with kidney injury. A single case of interstitial nephritis and reversible AKI in a patient treated with atazanavir has also been reported [153] Acute kidney injury attributed to ritonavir has been reported in several patients [154-157], the majority of whom were receiving concomitant nephrotoxic medications, while others had preexisting kidney disease or were volume depleted. In several patients, AKI recurred upon ritonavir rechallenge. Kidney biopsies were not performed, so histopathologic correlates and etiology of kidney injury were not precisely defined. [Pg.391]

Figure 4. Kidney biopsy demonstrates a diffuse cellular infiltrate within the interstitium with inflammatory cells including eosinophils (arrowhead) and lymphocytes. Tubulitis is present (arrow). Hematoxylin and eosin stain (H Ex 47)... Figure 4. Kidney biopsy demonstrates a diffuse cellular infiltrate within the interstitium with inflammatory cells including eosinophils (arrowhead) and lymphocytes. Tubulitis is present (arrow). Hematoxylin and eosin stain (H Ex 47)...
Aasebo W, Scott H, Ganss R. Kidney biopsies taken before and after sodium phosphate bowel cleansing. Nephrol DialTransplant 2006 22 920-922. [Pg.593]

Salomon Ml, PoonTP,Goldblatt M,TchertkoffV. Renal lesions in heroin addicts a study based on kidney biopsies. Nephron 1972 9 356-363. [Pg.610]

The situation where the CSA impact on native kidneys is most evident is the treatment of autoimmune diseases. In these patients rejection is not an issue, and the native kidneys are usually healthy and not submitted to other potential insults, making it easier to establish a direct cause-effect correlation. In fact, Feutren and Mihatsch, on behalf of the International Kidney Biopsy Registry of Cyclosporine in Autoimmune Diseases, found interstitial fibrosis and tubular... [Pg.640]

Although CSA has been used for treatment of other autoimmune diseases such as atopic dermatitis, myasthenia gravis, systemic sclerosis and primary biliary cirrhosis, data about chronic structural injury in these situations are scarce. There are occasional reports of end stage renal failure or development of interstitial fibrosis in kidney biopsies in demyelinat-... [Pg.643]

Renal morphology aftercyclosporin Atherapy in rheumatoid arthritis patients. International Kidney Biopsy Registry ofCyclosporin (Sandimmun) in Autoimmune Diseases. BrJ Rheumatol 1993 32Suppl 1 65-71. [Pg.674]


See other pages where Kidney biopsies is mentioned: [Pg.614]    [Pg.13]    [Pg.15]    [Pg.37]    [Pg.38]    [Pg.38]    [Pg.40]    [Pg.50]    [Pg.55]    [Pg.64]    [Pg.337]    [Pg.766]    [Pg.3597]    [Pg.384]    [Pg.385]    [Pg.386]    [Pg.572]    [Pg.606]    [Pg.642]    [Pg.645]    [Pg.645]   
See also in sourсe #XX -- [ Pg.3 , Pg.4 , Pg.25 , Pg.41 , Pg.47 , Pg.58 ]

See also in sourсe #XX -- [ Pg.111 ]




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