Reversible Renal Insufficiency Research Articles

Adding bendamustine to melphalan before ASCT improves CR rate in myeloma vs. melphalan alone: A randomized phase-2 trial

Definite cure remains exceptional in myeloma patients even after high-dose chemotherapy (HDCT) with melphalan (Mel) and autologous stem cell transplantation (ASCT). Thus, improving efficacy of HDCT in MM remains an unresolved issue. This randomized phase II trial compared standard 200 mg/m2 Mel HDCT to experimental HDCT with 200 mg/m2 bendamustine, given both at days −4 and −3, combined with 100 mg/m2 melphalan at days −2 and −1 (BenMel) before ASCT as first-line consolidation in myeloma patients. The primary endpoint aimed to identify at least a 15% improvement in the complete remission rate (stringent CR + CR) after HDCT with BenMel compared with Mel alone. A total of 120 MM patients were 1:1 randomized. The rate of sCR/CR after ASCT was higher in BenMel than in Mel treated patients (70.0% vs. 51.7%; p = 0.039). Three patients in the BenMel group (5.0%) had reversible acute renal insufficiency compared with none in Mel patients. Minimal residual disease negativity (<10-5) by flow cytometry was observed in 26 (45.6%) BenMel patients and 22 (37.9%) in the Mel group (p = 0.375). Our data suggest that BenMel HDCT is safe and improves the sCR/CR rate compared with standard Mel alone.

SCT for Secondary AML in a Patient with Glycogen Storage Disease Type 1b

AbstractAbstract 4402It is well established that patients with congenital neutropenia due to mutations of ELANE or HAX1 have a strongly increased risk of developing secondary leukemia. In contrast, the leukemia risk is not strongly increased in patients with specific other neutropenia subtypes (e. g. cyclic neutropenia with ELANE mutations). Here we report the first glycogen storage disease type Ib (GSD1b) patient in our registry who developed acute myelogenous leukemia (AML). GSD1b is an autosomal recessive disorder of glycogen metabolism with intracellular accumulation of glycogen caused by mutations in the glucose-6-phosphate translocase gene. Patients present with hepatomegaly, growth retardation, hypoglycemia, lactic acidosis as well as neutropenia and neutrophil dysfunction predisposing to bacterial infections. G-CSF has been shown to be an effective long-term treatment for GSD1b patients leading to an increase in neutrophil counts and enhancement of neutrophil function resulting in fewer infections and improved quality of life. The European Branch of the Severe Chronic Neutropenia International Registry (SCNIR) has collected long-term data from 23 patients with GSD1b. Median age was 17 years, 3 patients expired from infections at an age of 8; 9 and 26 years, respectively. All 23 patients received G-CSF treatment for a median duration of 9.5 years, 22 patients received continuous G-CSF with a median dose of 3.4 mcg/kg/day (range 0.8 to 5 mcg/kg/day), one patient received G-CSF interventionally only.Our patient was diagnosed with AML FAB classification M2 linked to cytogenetic aberrations involving trisomy 21. Leukemia cells also harboured a missense RUNX 1 mutation in exon 3. G-CSF treatment was initiated at age 5 months at a dose of 2.3 mcg/kg/d and was continued until AML diagnosis at age 10 years. The G-CSF dose was increased due to low ANCs and infectious episodes with otitis media and pneumonitis up to 4.05 mcg/kg/day. After initial AML treatment with a hypometylating chemotherapy consisting of azacytidine and cytarabine she developed partially reversible renal insufficiency and oxygen dependent pneumonitis which led to a reduction of chemotherapy despite persistence of AML blasts.Remission was achieved with the use of mylotarg. Subsequently, she received a conditioning regimen with melphalan, fludarabine and treosulfan plus ATG-Fresenius followed by infusion of 10/10 HLA matched peripheral blood stem cells from an unrelated donor. Leukocyte engraftment occurred on day +18 followed by neutrophil engraftment on day +21. Post-SCT she developed grade III skin GvHD on day +8 which was responsible to steroid treatment. Discussion:Up to date 3 GSD1b patients with development of AML have been reported in the literature. Two patients were on long-term G-CSF treatment (Pinsk et al. J Pediatr. 2002; Schroeder et al. J Medical Case Reports 2008), one patient transformed predating the availability of G-CSF (Simmons et al. J Pediatr. 1984). Conclusion:According to the literature, leukemic transformation in patients with GSD1b is a rare event. However, with a total of four patients reported with secondary AML with or without G-CSF treatment, GSD1b patients may have a higher leukemia risk than previously anticipated. Independent from G-CSF treatment, regular bone marrow examinations (morphology, cytogenetics, mutation analysis of candidate genes such as RUNX1) may help to detect malignant transformation early and therefore avoid chemotherapy prior to SCT. SCT is a treatment option for AML in GSD1b, but further data is required. Disclosures:No relevant conflicts of interest to declare.

Lenalidomide Followed with Donor Lymphocytes Infusion (DLI) After Allogeneic Stem-Cell Transplantation (Allo-SCT) with Reduced-Intensity Conditioning in Patients with High Risk Multiple Myeloma

Abstract 4310 Purpose:Relapse remains the main issue after allogeneic stem cell transplantation (Allo-SCT) in high risk Multiple Myeloma (MM) patients. The aim of this study is to assess the anti-myeloma effect of lenalidomide followed by donor lymphocyte infusion (DLI) as adoptive immunotherapy after transplantation. Patients and methods:Twelve patients with refractory and high risk myeloma were analyzed. Median age at transplantation was 56 years (46–64); 6 patients (50%) received lenalidomide before Allo-SCT. All patients received a RIC including Fludarabine 30 mg/m2 5 days, ATG 2,5 mg/kg for 2 days and Busilvex 3.2 mg/kg/day (3 days in 6 patients and 2 days in 6 patients). All but one received peripheral blood stem cells (PBSC). Donor was HLA id in 6 patients and matched unrelated in 6 patients. It is our standard long term practice to consider post-transplant DLI in patients with progressive or persistent disease after day 100 if no GVHD signs were evident. In 2010, we introduced the use of lenalidomide after day 100 in patients with MM presenting the same characteristics. Doses ranged from 10 to 25 mg/day. Lenalodomide treatment could be completed with DLI, administered afterward, at least after 2 cycles. Results:The median time between Allo-SCT and lenalidomide was 10 months (3–38). The median initial dose of lenalidomide was 15 mg (10–25). Patients received a median of 6 cycles (1–10). Nine patients (60%) received an escalating dose of DLI; 1 × 107/Kg of CD3+cells for the first DLI and 1 × 108/Kg of CD3+cells for the second DLI. One patient with GVHD (after tapering of the cyclosporine A and only after 10 days of lenalidomide) and two patients with progressive disease after lenalidomide did not receive DLI.The toxicity related to lenalidomide was mainly haematological (grade II in 4 patients (33%) and grade I in 3 patients (25%); 7 patients (58%) had moderate asthenia. One patient developed a reversible renal insufficiency after 10 cycles of lenalidomide, none of our patients developed thrombo-embolism under treatment.At the last follow up, 9 patients are alive and all of them are under ongoing treatment. Four patients achieved complete remission (CR) and five patients partial remission at last evaluation. The 1 and 2 years probability of the progression-free survival (PFS) was 75% and 50% and overall survival (OS) was 83 % and 69% respectively. The median OS was not reached and the median PFS was 23 months. Conclusions:These data show that lenalidomide has an acceptable toxicity. Combination with DLI should be further evaluated in a larger cohort of patients. Disclosures:No relevant conflicts of interest to declare.

Reversible Renal Insufficiency Secondary to Extrinsic Splenic Compression of the Kidney in a Patient with Chronic Lymphocytic Leukemia

While increased renal venous and direct renal parenchymal pressure may cause renal insufficiency, there are no prior reports of hypersplenism secondary to chronic lymphocytic leukemia (CLL) doing so. This first report of massive splenomegaly leading to marked compression of the left kidney associated with renal insufficiency that resolved after splenectomy illustrates that profound extrinsic renal compression from splenomegaly may significantly compromise left renal function and splenectomy should be considered in this situation.

Clinical characterization of first cycle reactions in patients with chronic lymphocytic leukemia treated with oblimersen

16514 Background: Serious adverse reactions during the first treatment cycle characterize many drugs used for chronic lymphocytic leukemia (CLL), including rituximab, alemtuzumab, flavopiridol, lenalidomide, and oblimersen. Termed cytokine release reactions (CRRs), these events have occurred more commonly in pts with bulky disease and elevated leukocyte counts, and some have been fatal. Rapid increases in serum levels of tumor necrosis factor-α, interleukin-6, interleukin-2, interferon-γ, and other cytokines may result in symptoms including fever, chills, nausea, vomiting, hypotension, and dyspnea. Ex vivo treatment of CLL cells with oblimersen induce release of vasoactive interleukin-8. First cycle reactions, including tumor lysis syndrome (TLS), proved dose-limiting in a phase 1–2 trial of oblimersen in pts with relapsed or refractory CLL. To characterize these reactions, we evaluated data from this single-agent study and from a phase 3 randomized clinical trial of oblimersen with fludarabine and cyclophosphamide (Flu/Cy). Methods: Data on investigator assessment of CRR and TLS were obtained from both studies, which included 155 pts; 40 were treated with oblimersen alone (3–7mg/kg/d by CIV for 5–7 days) and 115 with oblimersen (3 mg/kg/d × 7 days) in combination with Flu/Cy. Results: Of 145 pts treated with oblimersen 3mg/kg/d, either alone or with Flu/Cy, 2 pts (1.3%) experienced CRR and TLS, respectively. Two CRRs occurred in 10 pts treated with 4–7mg/kg/d. Reactions typically began 24–48 hours after starting treatment. CCR was usually associated with spiking fever, nausea, dehydration, rigors, and back pain. Rarely pts developed hypotension, acidosis, or reversible renal insufficiency, usually with a reduction in WBC. Symptoms lasted 1 day to several weeks (1 pt). In most cases, reactions were reversible with intensive supportive care, including IV fluids, pressors, and antibiotics; 1 death from TLS and 1 from CCR occurred during cycle 1. There was no definitive correlation with baseline measures of disease burden. Conclusion: First cycle oblimersen reactions are uncommon but represent a risk. Early symptoms (fever, nausea, and dehydration) require aggressive treatment, which may prevent progression of the reaction. [Table: see text]

Phase II Study of Timed Sequential Therapy (TST) with Topotecan, Cytosine Arabinoside (ARA-C), and Mitoxantrone (TAM) Induction Therapy Followed by Non-Cross-Resistant Consolidation Chemotherapy for Adults with Newly Diagnosed Acute Myelogenous Leukemia (AML).

Clinical results in AML continue to need improvement, particularly for age ≥60, prior MDS or secondary AMLs, and AMLs with adverse cytogenetics (CG) where complete remission (CR) rates are <50% and cure rates are <10%. In an attempt to improve these outcomes, we developed a TST regimen of the topoisomerase I inhibitor Topotecan with ara-C and Mitoxantrone (TAM) as induction therapy for adults with newly diagnosed AML: T, 4.5 mg/m2 IV continuous infusion (CI) over 72 hrs days (d) 1-3; A, 2 gm/m2 IV CI over 72 hrs d 3-5; and M, 40 mg/m2 IV d 10. CR patients with poor risk features received consolidation TST with T, 4.5 mg/m2 CI over 72 hrs d 1-3; A, 2 gm/m2 IV CI over 72 hrs d 3-5; and etoposide (E), 300 mg/m2 IV CI over 72 hrs d 10-12 (TAE); CR patients without poor risk features received consolidation TST with A, 2 gm/m2 CI over 72 hrs d 1-3 and 10-12; and idarubicin (I) 12 mg/m2 IV d 1,2,3 (AIA). From 04/02-2/04, 60 newly diagnosed AML patients (median age 49 yrs, 21–79) received TAM induction chemotherapy. Of 60 pts, 47 (78.5%) had at least one poor prognostic feature: age ≥60, 16 (27%); adverse CG, 28 (47%); MDS/AML, 10 (17%); secondary AML, 3 (5%); and/or WBC >25,000/μl, 23 (38.5%). Of the 41 (68.5%) pts who achieved CR, 32 (78%) received consolidation TST (22 TAE; 10 AIA). The remaining 9 pts received alloBMT (2), alternate therapy (5), or no consolidation (2) due to incomplete reversal of organ damage. Furthermore, 8 pts who finished 2 cycles of TST subsequently received alloBMT (3), autoBMT (2) and maintenance Zarnestra (3). Median overall survival (OS) for all pts is 10.1 mos, with 1yr survival 45.7% (95% CI; 32.5%–58.9%). On multivariate analysis, only antecedent MDS was a significant risk factor for poor OS (HR=2.5, 95% CI 1.13–5.65; p=0.02). For patients who achieved CR, median disease free survival (DFS) was 9.9 mos (95% CI; 5.8–18.2) with 1yr DFS 45.9% (95% CI; 29.4%–62.4%). Preceding MDS (p=0.02), adverse CG (p=0.04) and age ≥50 (p=0.06) were associated with low CR. Induction and consolidation mortality were <10%. Median time for ANC >100/μl was 28 days (22–56) and platelets >50,000/μl was 30 days (22–81) following TAM. For consolidation, median time to ANC >100/μl was 27.5 days (19–48) for TAE and 39 days (26–43) for AIA, and plts >50,000/μl 34 days (19–87) for TAE and 54 days (33–79) for AIA. Toxicities during induction and consolidation were generally ≤grade 3 and consisted of infection (bacteremias, pneumonias), oral and/or GI mucositis, transient elevation in liver function tests, reversible renal insufficiency. Pulmonary hemorrhage (1), GI bleed (3), CNS bleed/infarct (2) and decreased ejection fraction (2) occured during induction/consolidation but resolved. Causes of death during induction were sepsis/multiorgan failure (3), progressive fungal pneumonia (1), grade 5 marrow aplasia (1); during consolidation multiorgan failure (1), renal failure/sepsis (1), pulmonary hemorrhage (1). In summary, TAM induction for AML is associated with significant CR rates and acceptable toxicity, but did not appear to overcome the poor DFS and OS in a high-risk group of adults.

Combined modality treatment with full-dose chemotherapy and concomitant boost radiotherapy for advanced head and neck carcinoma

The purpose of this study was to evaluate the feasibility and efficacy of a treatment concept combining three cycles of full-dose chemotherapy (CT) with concomitant accelerated uninterrupted radiotherapy (RT). Twenty-three patients (median age: 54 years, range: 35-70) with locally advanced squamous cell carcinoma of the head and neck (SCCHN) were included. The primary tumor involved the hypopharynx (n=7), base of the tongue (n=10), nasopharynx (n=2) or upper esophagus (n=1) or its location was unknown (n=3). Treatment consisted of three cycles of chemotherapy (cisplatin 100 mg/m2 on day 1; 5-FU 1,000 mg/m2 per day for 5 days as a continuous infusion, preceded by amifostine 910 mg/m2), repeated every 3 weeks. Uninterrupted concomitant boost-accelerated RT (total dose of 70 Gy in 6 weeks) started together on day 1 of the second cycle. All but two patients received the full course of RT. Eighteen patients achieved complete remission (78%). At a median follow-up of 45 months the overall survival was 56% (95% c.i. 32-79%) and the loco-regional control 71% (95% c.i. 52-91%). Toxicity involved reversible renal insufficiency of > or = grade II in 9 patients (39%) and neutropenic fever in 9 patients (39%). All patients suffered from moderate to severe mucositis (grade II/III), and 19 patients presented cutaneous toxicity grade III. Concomitant boost-accelerated RT combined with concurrent full-dose cisplatin/5-FU chemotherapy and amifostine is feasible with manageable, although substantial, toxicity. The overall survival of 4 years is promising. Newer regimens causing less acute mucosal and skin toxicity are needed.

Kinetics of carbamylated haemoglobin in acute renal failure.

Carbamylation of proteins by isocyanic acid, the reactive form of cyanate derived from urea, is increased in uraemia and may contribute to uraemic toxicity. Kinetics of carbamylation that may reflect uraemic toxicity is not clearly defined in acute renal failure (ARF). Twenty-eight patients with ARF and 13 with chronic renal failure (CRF) were included in the study in order to determine changes in carbamylated haemoglobin concentration (CarHb) in ARF. The usefulness of this parameter for differentiating ARF from CRF was also investigated. CarHb was measured by high-performance liquid chromatography after acid hydrolysis. Mean CarHb level (expressed as microg carbamyl valine per gram (CV/g) Hb) was significantly higher in ARF (54.3+/-5.2) than in normal subjects (31.6+/-1.3). On admission, CarHb level was correlated with duration of ARF prior to hospitalization in the intensive care unit (r(2)=0.723, P<0.001). CarHb was significantly higher at recovery in the subgroup of patients requiring haemodialysis than in the subgroup not requiring haemodialysis (82. 4+/-11.3 vs 46.7+/-5.2, P<0.01). Similarly dialysis patients lost more weight (8.6+/-1.4 vs 2.7+/-0.5 kg, P<0.005) and had higher averaged blood urea levels in the 20 days prior to recovery (17. 6+/-1.9 vs 11.3+/-1.8 mol/l, P<0.05). After recovery, CarHb level decreased at a rate of 0.219 microg CV/g Hb per day in patients with reversible renal insufficiency. CarHb concentration was higher in patients with CRF. A cut-off CarHb value of 100 microg CV/g Hb had a sensitivity of 94% and a positive predictive value of 94% for differentiating ARF from CRF. Kinetics of CarHb showed a near normal red blood cell life span in ARF. Changes in CarHb enabled, with a good sensitivity, the distinction to be made between patients who recovered from ARF and those with sustained renal impairment, whether due to prior CRF or resulting from parenchymal sequelae. Measurement of CarHb is valuable at clinical presentation of ARF in patients with an unknown medical history of renal disease.

The Indispensability of Heme Oxygenase-1 in Protecting against Acute Heme Protein-Induced Toxicity in Vivo

Heme oxygenase (HO) is the rate limiting enzyme in the degradation of heme, and its isozyme, HO-1, may protect against tissue injury. One posited mechanism is the degradation of heme released from destabilized heme proteins. We demonstrate that HO-1 is a critical protectant against acute heme protein-induced toxicity in vivo. In the glycerol model of heme protein toxicity-one characterized by myolysis, hemolysis, and kidney damage-HO-1 is rapidly induced in the kidney of HO-1 +/+ mice as the latter sustain mild, reversible renal insufficiency without mortality. In stark contrast, after this insult, HO-1 -/- mice exhibit fulminant, irreversible renal failure and 100% mortality; HO-1 -/- mice do not express HO-1, and evince an eightfold increment in kidney heme content as compared to HO-1 +/+ mice. We also demonstrate directly the critical dependency on HO-1 in protecting against a specific heme protein, namely, hemoglobin: doses of hemoglobin which exert no nephrotoxicity or mortality in HO-1 +/+ mice, however, precipitate rapidly developing, acute renal failure and marked mortality in HO-1 -/- mice. We conclude that the induction of HO-1 is an indispensable response in protecting against acute heme protein toxicity in vivo.

Short-course, cost-effective treatment with amphotericin B-fat emulsion cures visceral leishmaniasis

Although short-course therapy with new lipid formulations of amphotericin B represents an advance over lengthy traditional treatments in visceral leishmaniasis (kala-azar), high cost has rendered these agents largely irrelevant in developing countries where the disease is endemic. Therefore, we tested standard amphotericin B deoxycholate mixed with a commercial fat emulsion as short-course treatment for Indian visceral leishmaniasis in Bihar in 1997/98. Seventy children and adults with splenic aspirate-documented infection, 23 of whom had failed prior antimony (Sb) therapy, received 5 alternate-day infusions of 2 mg/kg. Apparent cure, which required a parasite-free splenic aspirate smear, was assessed 20 days after treatment (day 30); definitive cure was determined at 6 months. Other than anticipated infusion-related fever and/or chills, treatment was safe and well tolerated. One patient required dose modification because of mild, reversible renal insufficiency. Sixty-nine patients (98·6%, CI 92·3–100%) had apparent cures; during follow-up, there were 4 treatment failures (relapses, 3; unrelated death, 1), yielding definitive cures in 65 of 70 patients (92·9%, CI 84·1–97·6%). Including retreatment costs for patients in Bihar (who now often fail initial Sb therapy), the final per patient cost of the tested regimen (US $260) was 59% and 43% less than treatment with Sb or conventional amphotericin B alone, respectively. Short-course treatment with amphotericin B-fat emulsion is active, cost-effective treatment for patients with visceral leishmaniasis including those with Sb-unresponsive infection.

ANTIPROTEINURIC EFFECT OF CALCIUM ANTAGONISTS ON PUROMYCIN-INDUCED EXPERIMENTAL NEPHROSIS

Calcium antagonists have a potential for beneficial effects on kidney function unrelated to their antihypertensive action. In this study we have investigated the efficacy of calcium antagonists compounds (verapamil, nifedipine and diltiazem) on reversible acute renal insufficiency, proteinuria and interstitial nephritis induced by the puromycin ammo nucleoside (PAN). An increase in blood pressure (BP) was detected on day 14, with no statistical differences in the response to calcium antagonists. Serum creatinine concentration increased to 1.2 mg/dL on day 7 after PAN and decreased to 0.7 mg/dL at 14 days, calcium antagonists shortened the time required to reach baseline or control levels. Calcium antagonists also reduced proteinuria in the PAN-treated animals, in both day 7 and day 14. Differential effects of the antagonists were observed. Verapamil caused a greater reduction (p < 0.01) in proteinuria than nifedipine or diltiazem in day 7. Moreover, verapamil (p < 0.01) and nifedipine (p < 0.01) reduced the total number of interstitial infiltrating leukocytes from 690 to 120 and 425 positive cells/20 high power fields (× 63) respectively, by contrast, diltiazem had no effect. We conclude that in this model of PAN nephropathy verapamil is more effective in reducing both proteinuria and the severity of acute interstitial nephritis than either nifedipine or diltiazem. The possible clinical implications of these results remain to be elucidated.

Intravenous immunoglobulin reduces anti-HLA alloreactivity and shortens waiting time to cardiac transplantation in highly sensitized left ventricular assist device recipients.

Recipients of left ventricular assist devices (LVADs) develop prominent B-cell hyperreactivity. We investigated the influence of anti-HLA antibodies on waiting time to cardiac transplantation in LVAD recipients and compared the effects of 2 immunomodulatory regimens on anti-HLA serum reactivity. Fifty-five previously nonsensitized LVAD recipients of a TCI device implanted between 1990 and 1996 were studied. Patients with anti-HLA antibodies received monthly courses of either intravenous immunoglobulin (IVIg) or plasmapheresis, in conjunction with cyclophosphamide. The effects of these regimens on anti-HLA alloreactivity and waiting time to transplantation were then determined by Kaplan-Meier log-rank statistics, nonparametric Wilcoxon rank-sum test, and Student's t test. Prolongation in transplant waiting time was related to serum IgG anti-HLA class I alloreactivity. Infusion of IVIg (2 g/kg) caused a mean reduction of 33% in anti-HLA class I alloreactivity within 1 week. Waiting time to transplantation was significantly reduced by IVIg therapy and subsequently approximated that in nonsensitized patients. Side effects of IVIg (2 g/kg) were minimal and related primarily to immune complex disease. Although plasmapheresis caused a similar reduction in alloreactivity to IVIg, this effect was achieved after longer treatment. Moreover, plasmapheresis was associated with an unacceptably high frequency of infectious complications. In patients resistant to low-dose (2 g/kg) IVIg therapy, high-dose (3 g/kg) IVIg was effective in reducing alloreactivity but was associated with a high incidence of reversible renal insufficiency. These results indicate that IVIg is an effective and safe modality for sensitized recipients awaiting cardiac transplantation, reducing serum anti-HLA alloreactivity and shortening the duration to transplantation. The therapeutic and safety profile of IVIg would appear to be superior to plasmapheresis.

Non-steroidal anti-inflammatory drugs and renal function.

The use of non-steroidal anti-inflammatory drugs (NSAIDs) is associated with a range of renal effects, including interference with fluid and electrolyte homoeostasis. Common adverse effects are generally mild and transient; less common but more severe effects include reversible renal insufficiency, interstitial nephritis and papillary necrosis. Any of these effects can influence the clinical course of patients at risk because of illness, debility or age. Acute renal failure associated with NSAID use has been reported to account for up to 15.6% of cases of drug-induced renal failure. NSAID-induced haemodynamic renal failure is virtually always reversible with appropriate management; the relatively rare complications of interstitial nephritis and papillary necrosis are more often irreversible. NSAID-related impairment of kidney function is probably due in large part to inhibition of prostaglandin synthesis. Use of a prostaglandin E1 (PGE1) analogue has been suggested to prevent some of the adverse renal effects of NSAIDs in patients at high risk, an interesting possibility that deserves further evaluation.

Hemolytic Effect of the Amplatz Thrombectomy Device

The hemolytic effect of the Amplatz thrombectomy device (ATD) was evaluated in nine dogs and in nine patients. The device was activated for 1-2 minutes in the abdominal aorta, inferior vena cava, or femoral artery of nine dogs. The device was activated for 1-4 minutes in the nine patients in occluded lower extremity bypass grafts (n = 5), native superficial femoral artery (n = 1), a pulmonary artery embolus (n = 1), a portocaval shunt (n = 1), and an iliac vein stent (n = 1). Patients were examined for laboratory evidence of hemolysis following mechanical thrombectomy. In all dogs haptoglobin level decreased, free hemoglobin level in the plasma increased, and hemoglobinuria was present. There was no change in renal function. The level of haptoglobin decreased and the level of plasma free hemoglobin increased in eight patients, with hemoglobinuria detected in one. More hemolysis was observed in the animals than in the patients. The ATD has a definite transient hemolytic effect. Until further studied, it should not be used in children and should be used with caution in patients who are anemic, hypoxemic, or have potentially reversible renal insufficiency. Activation time should be monitored closely because hemolysis probably increases with increasing activation time.

Glomérulonéphrite extracapillaire au cours d'un traitement par interféron alpha

We report here on a patient who had reversible acute renal insufficiency after being treated with interferon-alpha for chronic mycloid leukemia.

Hypercalcemia, Hypernatremia, and Reversible Renal Insufficiency

Hypercalcemia, Hypernatremia, and Reversible Renal Insufficiency

Studies within Studies

Excerpt To the Editors:Drs. Toto and colleagues (1) recently described eight patients who had reversible renal insufficiency that was attributed to the use of an angiotensin-converting enzyme inhib...

Reversible Renal Insufficiency and Angiotensin-Converting Enzyme Inhibitor Therapy

Excerpt To the Editors:Toto and colleagues (1) reported a relatively high incidence of reversible renal insufficiency (19%) in patients with hypertensive nephrosclerosis and chronic renal insuffici...

Minor degree of reversible renal insufficiency: a frequent complication of adult minimal-change nephrotie syndrome

We report on a group of 27 patients with minimal-change nephrotic syndrome who presented complete recovery from the nephrotic syndrome and the other clinical signs during follow-up. At the start of the examination an elevated serum urea was found in 10 (37%) and of serum creatinine in 4 (15%) patients. Creatinine clearance was decreased in 10 (37%), systolic blood pressure was elevated in 8 (29%) and diastolic in 11 (41%). Interstitial oedema was found in 3, tubular parenchymal degeneration in 4, slight interstitial mononuclear infiltration in 6 and slight interstitial fibrosis in 1 patient. Complete recovery of renal function was seen in all patients.

Morphine Intoxication during Acute Reversible Renal Insufficiency

Morphine Intoxication during Acute Reversible Renal Insufficiency