Nonsecretory multiple myeloma - a rare case of acute renal failure.

Multiple myeloma (MM) is a plasma cell dyscrasia accounting for 10% of all hematologic malignancies. Diagnosis is based on histologic, serologic and radiographic features. The nephrotoxic manifestations of immunoglobulin light chain overproduction are the most common cause of renal function impairment. The most frequent renal lesion is "cast nephropathy" and results from immunoglobulin light chain nephrotoxicity. MM very rarely produces diffuse bilateral renal infiltration. We report the interesting case of a patient with non-secretory myeloma, who presented with acute renal failure and increased kidney size due to massive renal infiltration by plasma cells. Pulse steroid therapy lead to rapid renal function improvement and reduction in kidney size. Renal failure is a frequent manifestation of MM, which can affect kidneys in several ways. MM should be included in the differential diagnosis of every case of unexplained renal failure, especially in the elderly, even in the absence of an M spike in serum and urine electrophoresis.

Prospective monitoring of BK virus replication in renal transplant recipients.

BACKGROUND: BK virus-associated nephropathy (BKVAN) can be diagnosed only with renal graft biopsy. Definitive diagnosis of BKVAN requires demonstration of BK virus (BKV) replication in renal allograft tissues. Non-invasive analysis of urine and blood is considered essential in screening renal transplant recipients. PATIENTS AND METHODS: This study evaluated prospectively the replication of BKV in plasma and urine with qualitative and quantitative real-time polymerase chain reaction in 32 de novo (group A) and 34 chronic (group B) renal transplant recipients and the long-term impact on graft function. RESULTS: In group A, 456 samples (228 plasma, 228 urine) were examined and BKV was detected in 31 (31/228, 14%) samples of plasma and 57 (57/228, 25%) samples of urine in 20 (20/32, 62.5%) and 23 (23/32, 72%) recipients, respectively. Incidence of viremia and viruria increased during the first 6 months presenting a peak the third postoperative month (viremia: 28% and viruria: 31%). Immune suppressive treatment with tacrolimus showed significant relation with viremia. Renal graft function in de novo renal transplant recipients remained stable throughout the follow-up period without influence of BKV replication. In group B, incidence of viremia and viruria were 3% (1/34) and 9% (3/34) correspondingly, indicating that after the first post-transplant year the risk of BKV re-activation is diminished. CONCLUSION: The highest incidence of BK viremia and viruria is observed the third post-transplantation month, confirming previously published studies in Europe and the United States, and long-term follow up shows that BKV replication decreases significantly after the third post-transplant month and even transient viremia or viruria does not have an impact on renal function.

Prospective study of urine cytology screening for BK polyoma virus replication in renal transplant recipients.

OBJECTIVE: BK virus (BKV) may be associated with interstitial nephritis in renal transplant recipients and this can lead to irreversible chronic allograft dysfunction. Early diagnosis of BKV nephropathy determines its progress because no specific antiviral therapy exists. Urine cytology, detection of viral DNA in urine or blood and renal biopsy are the main diagnostic tools. The purpose of this study was to evaluate the use of urine cytology for diagnosis of BKV replication in renal graft recipients. PATIENTS AND METHODS: We studied 32 de novo renal transplant recipients prospectively with sequential urine samples for a period of 1 year. Thin-Prep methodology was used to prepare the slides. Cytology results were correlated with polymerase chain reaction (PCR) in urine and blood. RESULTS: Decoy cells indicative of BKV infection were detected in 14 (7.3%) of the 190 urine samples derived from 11 recipients. In three cases with positive decoy cells, BK viraemia and viruria were simultaneously identified. In a further three cases, BKV active replication was confirmed in urine by both cytology and PCR. CONCLUSIONS: Urine cytology is an easy and rapid method of detecting decoy cells in cases where renal biopsy is not possible. However, the low incidence of detection of decoy cells in the present study, together with poor correlation with PCR results, questions its sensitivity and specificity in diagnosing BKV reactivation.

Hypercalcemia due to resistant hyperparathyroidism in renal transplant patients treated with the calcimimetic agent cinacalcet.

INTRODUCTION AND AIMS: Calcimimetic agents increase the sensitivity of calcium-sensing receptors of parathyroid glands and suppress both serum calcium levels and parathyroid hormone (PTH). The use of these drugs in patients with a functioning graft suffering from resistant hyperparathyroidism and hypercalcemia is still under investigation. We report seven patients who were treated with the calcimimetic agent cinacalcet. METHODS: The four male and three female patients of 38 to 72 years of age received a renal transplant from 4 to 35 months before cinacalcet treatment. Serum creatinine was 1.2 to 1.8 mg/dL (estimated glomerular filtration rate between 40 and 75 mL/min). Immunosuppressive treatment consisted of interleukin-2 antibody induction therapy, calcineurin inhibitors (cyclosporine or tacrolimus), prednisolone, and mycophenolate mofetil. Mild to severe hyperparathyroidism resistant to vitamin D analog treatment (intact parathyroid hormone molecule [iPTH] 174 to 519 pg/mL) was accompanied by severe hypercalcemia (Ca >11 mg%). To date the patients have completed 3 to 18 months of therapy. Cinacalcet 30 mg/d was initially administered. RESULTS: This treatment resulted in a rapid decrease in total serum calcium (8.6 to 9.2 mg/dL) while PTH showed a milder, progressive decrease. Having controlled calcium levels, 1alpha OH vitamin D (0.25 microg/d per os) was added to the treatment, which resulted in a further decline of iPTH without producing an increase in serum calcium concentrations (median initial iPTH value 401 pg/mL, median value after treatment 176 pg/mL). Therapy was well tolerated without hypocalcemic events. CONCLUSION: Cinacalcet offered a better holistic treatment approach to such patients.

Treatment of severe hypercalcemia due to refractory hyperparathyroidism in renal transplant patients with the calcimimetic agent cinacalcet.

Calcimimetic agents increase the sensitivity of calcium sensing receptors of parathyroid glands and suppress both serum calcium levels and parathyroid hormone. There are still limited data on the treatment of renal transplant patients with severe hypercalcemia and hyperparathyroidism with calcimimetics (cinacalcet). We describe two such renal transplant patients with chronic kidney disease Stage 3 who presented with persistent hypercalcemia (serum calcium 11.5-12 mg/dl) and refractory hyperparathyroidism (iPTH 194-547 pg/ml). Control of hypercalcemia with cinacalcet (serum calcium <10 mg/dl) resulted also in an improvement of hyperparathyroidism, but with a slower rate than that of the lowering of serum calcium. Addition of a vitamin D analog together with the calcimimetic agent resulted in faster control of the resistant hyperparathyroidism in both patients (iPTH <145 pg/ml) with clinical improvement and without any side effect. It seems that this new agent will improve our clinical approach of renal bone disease permitting a more integrated and successful treatment of hyperparathyroidism and its consequences on patients with chronic kidney disease.

Severe acute renal failure in a 19-year-old woman following laparoscopic cholecystectomy.

A case of severe acute renal failure in a young female patient necessitating renal replacement therapy after laparoscopic cholecystectomy is described. The histology of the renal lesion assigned to the effects of laparoscopic surgery is relevant for the pathogenesis of renal complications after such procedures. This explains part of the pathogenesis of the ischemic lesions in kidney structure that increased intra-abdominal pressure can provoke. Emphasis is given on the prevention of such side effects.

Transplantation of pediatric kidneys to adult recipients: an analysis of 13 cases.

INTRODUCTION: The shortage of cadaveric donors for kidney transplantation has prompted many centers to expand the criteria used for donor selection to increase the organ supply. The use of cadaveric pediatric kidneys has been suggested as a means to overcome the shortage. However, some studies indicate that kidneys from pediatric donors show inferior results to those from adult donors. In this retrospective study we examined the outcome of kidney transplantation using cadaveric pediatric donors. MATERIALS AND METHODS: From October 1990 to May 2002, 13 adult patients received pediatric renal transplants including two that were transplanted en bloc. The patients were divided into two groups based upon donor age: group I donors were 18 months to 6 years old; the seven recipients were of mean age 47.3 years. Group II donors were 7 to 15 years old; the six recipients were of mean age 43.6 years old. Cyclosporine-based immunosuppressive regimens were used in both groups. RESULTS: The patient survival rate was 85.7% in group I and 100% in group II. The graft survival rates at the first and third posttransplant year in group I were 71.4% (5/7) and 57.1% (4/7) and in group II, 66.7% and 50%, respectively. The frequency of urinary complications in group I was 28.5% (2/7) and in group II 33.3% (2/6). There was one case of venous thrombosis in group II. CONCLUSION: Pediatric renal grafts may be used with reasonable safety. However, surgical complications remain a significant problem especially with younger pediatric grafts.

Long-term control of hypertension in dialysis patients by low dose atenolol.

Hypertension in dialysis patients is considered a major factor in cardiovascular mortality. We investigated long-term efficacy of intermittent atenolol (AT) administration in 10 (7M/3F) hypertensive dialysis patients, age 60.5 (38-72), on dialysis for 56.5 months (8-156) thrice per week (10.5-13.5 h/w) (A). A similar group of 11 normotensive patients served as controls (B). Hypertension was defined as BP> 140/90 (day) and >120/80 mmHg (night) by a 44-h ambulatory BP monitoring (ABPM) after the mid-week session. Dialysis ultrafiltration, hematology, biochemistry were similar in A and B. Atenolol was started on an alternate day, 37.5 mg/w and increased as needed. After 34 days (6-80) and a dose of 68.75 (37.5-450) mg/w, BP dropped (ABPM: MAP 104+/-11.5 to 95.6+/-10.4 mmHg, P=0.0025) similar to controls and daytime HR dropped: 84.6+/-9.2 to 69.3+/-8.2, P=0.0008 and at night: 79.5+/-7.6 to 68.6+/-8.6 b/1' becoming lower than in B: 83+/-10.8/69.3+/-8.2, P=0.009 and 80.5+/-11.7/68.6+/-8.6 b/1' (P=0. 02). Six months later ABPM in A as well as echocardiography in A and B remained unchanged. Moderate, volume independent hypertension in stable dialysis patients is easily controlled during the interdialytic period by small intermittent atenolol doses.

Insulin and mineralocorticoids influence on extrarenal potassium metabolism in chronic hemodialysis patients.

Insulin-mineral corticoids effects on extrarenal K+ metabolism in dialysis patients. During the inter-dialytic interval in dialyzed patients, hydrogen and potassium ions are regulated by extrarenal mechanisms. We studied the hormonal and acidotic effects on the extrarenal potassium metabolism, in selected, anuric and stable, hemodialysis patients. Fifteen patients, were grouped according to the mean mid-week pre-dialysis K+ over the past 12 months: > 6.0 mEq/L (G1, n=5), = 5.1-6.0 mEq/L (G2, n=5), < or = 5.0 mEq/L (G3, n=5). After a mid-week hemodialysis session and 12 h fasting, they received 1 g/Kg glucose p.os (A). Insulin, aldosterone, renin, pH, HCO3-, glucose, body weight, blood pressure and heart rate were measured before and 60' after the meal. We recorded the same parameters, except insulin, in 15 patients, similarly grouped, before hemodialysis (T0) and on 3 consecutive off dialysis days (T1-T3); G1 received fluorohydrocortisone (FHC) 0.1 mg-0.3 mg/day, according to body weight and G3 spironolactone (SLT) 200 mg per day. G2 were controls (B). (A) A significant rise in glycemia (81 +/- 23 to 157 +/- 52 mg/dL, P<0.001) and insulin (11.8 +/- 6.2 to 46.8 +/- 19.5 microU/mL, P<0.001), with a drop in K+ (5.1 +/- 0.6 to 4.8 +/- 0.7 mEq/L, P=0.001) and aldosterone (453 +/- 373 to 383 +/- 364 pg/mL, P<0.01), were noted at T60 vs. T0, in all groups. Insulin levels correlated negatively (r=-0.54, P<0.04) to serum K+ at T60, in all patients. (B) No major pH, HCO3 and aldosterone changes were observed in the 3 groups. Despite that, K+ dropped in G1 by FHC (6.7 +/- 0.9 to 5.9 +/- 0.6 mEq/L, P<0.05), rose in G3 by SLT (4.4 +/- 0.4 to 5.4 +/- 0.3 mEq/L, P<0.05) and remained unchanged in controls (5.8 +/- 0.2 to 5.8 +/- 0.6 mEq/L), (T0 vs T3 pre-dialysis values). Glucose significantly lowered K+ by promoting adequate insulin secretion. Drugs affecting aldosterone action significantly influenced potassium metabolism. Acid-base balance was not important in K+ handling in steady state anuric dialysis patients.

Lower long-term efficiency of intradermal hepatitis B vaccine compared to the intramuscular route in hemodialysis patients.

Intramuscular (i.m.) and Intradermal (i.d.) vaccination against hepatitis B (HB) are efficient in hemodialysis patients. We retrospectively analysed the response of 32 patients during 48 consecutive months and compared the results of the two vaccination routes using the recombinant vaccine (Engerix, SKB). Thirteen patients were vaccinated with 5 mcg i.d. every 2 weeks (total 8 doses), plus an i.m. dose on month (M) 12 (group A). Nineteen patients (group B) were vaccinated with 4 i.m. doses of 20 mcg each, on months M0, 1, 2 and 12. HB antibodies were measured on M5, M11, M13, M24, M36 and M48. An additional 20 mcg i.m. dose was given with titers below 10 mIU/ml. Seroconversion, seroprotection and antibody levels were equivalent in both groups up to M13; with the exception of seroconversion rates, a significantly different response was observed afterwards (A/B, in mIU/ml): M5: 399 +/- 107 vs 342 +/- 69, M13: 536 +/- 118 vs 673 +/- 61, M24: 278 +/- 94 vs 595 +/- 81, P=0.02, and M48: 68 +/- 29 vs 565 +/- 92, P=0.003. Early HB(S)AB levels did not correlate with those found four years later in both groups. An additional booster dose was given 8 times in 4 group A patients (1-3 doses/patient) and 3 times in 1 group B patient. Immune response to HB vaccine in hemodialysis patients is initially equivalent by both immunization routes. Late antibody titers were found significantly lower in i.d. immunization with more frequent booster doses needed.

Long-term effects of small doses of calcitriol in hemodialysis patients with moderate secondary hyperparathyroidism.

Prevention of secondary hyperparathyroidism (SHPTH) and treatment of the moderate cases by small p.os doses of Vitamin D has not been thoroughly investigated on the long term, while large doses of Vitamin D have been successful in the short term treatment of this entity. We administered calcitriol p.os 0.5-1.0 microgram, according to iPTH levels, after each dialysis session, in 19 patients (group A) for 36 months. They were ten men and nine women, 63 years old (43-81), with iPTH levels > 4N (419 +/- 185 pg/mL). Seven adenomas were found in five of them (group A1). Serum Ca, phosphate (P) and alkaline phosphatase (AP) were measured every 15-30 days. Serum iPTH and aluminum as well as echogram or scanning of the parathyroid glands were checked every 6 months. Ten additional dialysis patients, seven men and three women, 54.5 years old (36-68), non-significantly different to group A in iPTH levels (290 +/- 225 pg/mL) with three adenomas in two of them (group B1) received no calcitriol and served as controls (group B). Calcitriol treatment significantly lowered serum iPTH levels in group A patients (from 419 +/- 185 to 173 +/- 142 pg/mL, p < 0.0001, delta iPTH: -246 +/- 161 pg/mL); iPTH remained stable in group B patients (delta iPTH: +7.9 +/- 116 pg/mL) with an intergroup significant difference at P < 0.0001. All other parameters measured did not show any significant change. No significant correlation of iPTH to Ca, P or AP was found in A. Initial iPTH levels were higher in A1 and B1 patients and decreased by calcitriol in A1 group. Adenomas in A1 patients did not change in number and size in contrast to B1 where new adenomas appeared (5 patients, 10 glands). Small doses of vitamin D lower high iPTH levels and prevent parathyroid gland hyperplasia. Existing hypertrophy is stabilized under calcitriol treatment both morphologically and biologically.