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Biomedical subjects

C Ponticelli

Publications and source records attributed to C Ponticelli.

At least 127 records · Page 7Linked to original sources
PubMed1994

Clinical features and course of Kaposi's sarcoma in kidney transplant patients: report of 13 cases.

We retrospectively evaluated the prevalence of Kaposi's sarcoma (KS) in 820 kidney transplant recipients with a follow-up period of at least 6 months. Thirteen patients developed a KS (1.6%): 2 were under conventional therapy and 11 under ciclosporin A. The onset of KS was 38.7 +/- 38.3 (range 6-124) months after transplantation in the whole population and after 33.9 +/- 19.7 months in the patients treated with ciclosporin A only. Nine were men and 4 women (male/female ratio: 2.25:1). The mean age at KS occurrence was 36.8 +/- 11.1 years. The mean follow-up period since KS diagnosis was 35.9 +/- 19.5 months. Clinical manifestation and severity of KS were heterogeneous: 5 patients had a KS with cutaneous involvement only, 8 patients a KS with multiple skin and mucosal and/or visceral lesions. Only 2 patients from the second group died of peritonitis due to intestinal lesions. In these 2 patients, immunosuppressive therapy had either been increased or reintroduced after a partial regression of KS. In all other patients, therapy was promptly reduced or withdrawn. In 1 patient local radiation therapy plus intralesional bleomycin administration were started and 1 patient received intralesional vincristine. Nine patients had a complete and 2 a partial remission of lesions. After therapy reduction, 4 patients lost their kidney (these patients however, had an already ongoing chronic rejection at KS diagnosis), in 2 there was an improvement of graft function, and in the other patients it remained stable. Our experience confirms that in most cases reduction or withdrawal of immunosuppression halts the evolution of both cutaneous and visceral lesions, without compromising graft function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

The history of urinary microscopy to the end of the 19th century.

In the 17th and 18th centuries, several authors performed urinary microscopy occasionally and were often unable to give their observations a practical diagnostic application. Such men included De Peiresc, Boerhaave, Ledermüller and Galeazzi. In the 1st half of the 19th century, however, urinary microscopy began to be used systematically. Rayer and Vigla identified for the first time elements other than crystals in urine and contributed to the methodology of handling samples for microscopy. Becquerel described dysmorphic erythrocytes, and Simon and Henle observed casts in urine and in histological preparations. In contrast, Bird mentioned casts only in passing, though he described many other elements and published the first complete book on urinary microscopy. The 2nd half of the 19th century was characterized by further advances, and in the book of Beale tubular cells were distinguished from other epithelial cells. Different types of casts were also linked with different renal diseases. By 1875 the classification of casts was complete. The work of the 19th century microscopists culminated in Rieder's book on clinical microscopy, which described each element of urinary sediment through 36 beautiful chromolithographic plates.

England↗
PubMed1994

High prevalence of silent gallstone disease in dialysis patients.

Gallstone disease was detected in 28% of 119 patients on regular dialysis treatment. The disease was silent in 82% of the patients. Stones were radiolucent in 88% of the cases, radioopaque in 8% and mixed in 4%. Among 49 variables considered, increasing age was the only variable that correlated significantly with increasing prevalence of gallstone disease. Since no relationships were found between gallstones and age or modes of dialysis, it is conceivable that some mechanism(s) linked with the preexisting chronic nephropathy might have been involved in the development of cholelithiasis. End-stage renal disease could be another so far unrecognized risk factor for cholelithiasis.

Adult↗
PubMed1994

Renal replacement therapy in cryoglobulinaemic nephritis.

Seventeen patients with nephritis due to mixed cryoglobulinaemia were submitted to regular haemodialysis in 11 and continuous ambulatory peritoneal dialysis in six after 145 +/- 55 months from the onset of the disease. Four patients with very poor clinical conditions died within 6 months from the beginning of dialysis. The other 13 patients were followed for a mean period of 78.7 +/- 41.6 months. The actuarial survival rate was 65% at 5 years. Both clinical and immunological signs of mixed cryoglobulinaemia reduced during dialysis but a long-lasting burn out was observed only in one patient. Two patients received a kidney graft. Mixed cryoglobulinaemia nephritis recurred in both of them respectively 5 and 10 months after transplantation. One patient lost his graft 13 months after transplantation because of chronic rejection. The other one still has a functioning kidney 48 months after renal transplantation. The life expectancy with dialysis for mixed cryoglobulinaemia patients is similar to that of patients with standard primary renal disease but some few patients with severe disease at the beginning of dialysis have a poor prognosis. Nephritis may recur after renal transplantation but this does not preclude per se a favourable course in the long term.

Actuarial Analysis↗
PubMed1993

Hepatorenal syndrome. New perspectives in pathogenesis and treatment.

Hepatorenal syndrome is a life-threatening complication of severe liver disease. It is generally accepted that the syndrome is the final stage of complex hemodynamic derangements associated with portal hypertension, ie, peripheral arterial vasodilation, effective hypovolemia, and hyperkinetic status. In spite of reduced systemic resistances, intrarenal vascular resistances are increased. This is probably the consequence of the activation of systemic vasoactive factors, such as the renin-angiotensin system, the sympathetic nervous system, and vasopressin aimed at restoring arterial filling pressure. Recently, it has been shown that intrarenal vasoconstrictors, such as leukotrienes and endothelins, are activated with the progression of liver disease. The renal vasoconstriction is counterbalanced by the intrarenal hyperproduction of vasodilating prostaglandins and kallikreins. When this balance is lost, for whatever mechanism, the renal vascular resistances dramatically increase and the hepatorenal syndrome develops. In spite of increased knowledge about pathogenesis, the treatment of hepatorenal syndrome remains unresolved. Low-dose dopamine or ornipressin are currently employed in many liver units to avoid further deterioration of renal function in patients with severe liver disease who are waiting for liver transplantation that remains, at present, the only effective treatment for hepatorenal syndrome.

Hepatorenal Syndrome↗
PubMed1993

Hypertension after renal transplantation.

In 212 cyclosporine-treated renal transplant recipients with stable graft function at 1 year and with potential follow-up of 5 years the prevalence of arterial hypertension was 81.6% at 1 year and 81.2% at 5 years. The logistic regression analysis showed that the presence of hypertension before transplantation (P = 0.0001; odds ratio 3.5), a plasma creatinine level higher than 2 mg/dL at 1 year (P = 0.0001; odds ratio 3.8), and a maintenance therapy with corticosteroids (P = 0.008; odds ratio 3.3) were positively associated with hypertension at 1 year after transplantation. The mean number of graft failures between 1 and 5 years was significantly higher and the mean reciprocal of plasma creatinine was significantly worse at 1 and 5 years in patients with noncontrolled hypertension than in normotensive patients or in patients with hypertension well controlled by drugs. We also investigated the potential protective role of nifedipine. The episodes of acute tubular necrosis (four versus three), of acute rejections (28 versus 29), the mean arterial pressure at 1 year (105 +/- 9 versus 104 +/- 9 mm Hg) and 5 years (105 +/- 10 versus 108 +/- 12 mm Hg), and the mean plasma creatinine level at 1 year (1.4 +/- 0.4 versus 1.6 +/- 0.4 mg/dL) and 5 years (1.8 +/- 1 versus 1.9 +/- 1 mg/dL) were similar in 52 patients who were given nifedipine for at least 4 years and 58 hypertensive patients who never took calcium channel blockers.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

A randomized trial of cyclosporine in steroid-resistant idiopathic nephrotic syndrome.

To compare the efficacy (induction of remission) and safety of cyclosporine (CsA) with those of supportive therapy in patients with steroid-resistant idiopathic nephrotic syndrome (INS), we organized an open, prospective, randomized, multicentric, controlled study for parallel groups, stratified for adults and children. Forty-five patients with steroid-resistant INS were randomly assigned to supportive therapy or CsA (5 mg/kg/day for adults, 6 mg/kg/day for children) for six months, then tapered off by 25% every two months until complete discontinuation. Four patients were lost to follow-up. During the first year 13/22 CsA-treated patients versus three of 19 controls attained remission of the nephrotic syndrome (P < 0.001). A symptom score was assessed at time 0 and at six months. The mean score significantly decreased in the CsA group (P < 0.001), but remained unchanged in the controls. At month 6 the mean urinary protein excretion, the mean serum proteins and plasma cholesterol had significantly improved in the CsA group but were not changed in the controls. There were no significant differences in serum creatinine and creatinine clearance between treatments (interaction time* treatments, P = 0.089 and P = 0.935, respectively) at month 6 versus basal. The CsA-related side-effects were mild; no significant difference in blood pressure between the two groups was seen at any time. This study shows that CsA can bring about remission in some 60% of patients with steroid-resistant INS. In patients with normal renal function and without severe hypertension, CsA at the therapeutic scheme adopted did not produce severe renal or extrarenal toxicity.

Adolescent↗
PubMed1993

Cyclosporine in idiopathic nephrotic syndrome.

Idiopathic nephrotic syndrome encompasses two main forms of glomerular diseases, minimal change nephropathy and focal segmental glomerulosclerosis. Minimal change nephropathy is a disease of children which generally responds to corticosteroids. After remission, however, many patients show frequent relapses or steroid dependency. In these patients, cyclosporine may obtain remission of proteinuria in 80% of cases, although relapse usually occurs when the drug is stopped. Focal glomerulosclerosis is generally resistant to corticosteroids. Under cyclosporine some 40% of patients may attain complete or partial remission of the nephrotic syndrome particularly if low-dose prednisone is associated. Relapse of proteinuria usually occurs after stopping the drug. As cyclosporine may expose to chronic nephrotoxicity some guidelines should be followed to prevent this complication: - the doses should not exceed 5 mg/Kg/day - they should be adjusted whenever an increase in plasma creatinine of > or = 30% over the baseline values occurs - treatment should be stopped if there is no response within 3 months - a careful monitoring of patient under the supervision of a clinician trained with the use of cyclosporine is necessary. The term idiopathic nephrotic syndrome (INS) defines the association of a nephrotic syndrome with non specific glomerular lesions, in the absence of immune complex deposition (1). On the basis of renal histology two main types of INS are recognized: minimal change nephropathy (MCN) and focal and segmental glomerular sclerosis (FSGS).

Adult↗