[Lupus glomerulonephritis: a long-term follow-up]. / Glomerulonefrite lúpica: estudo da evolução a longo prazo.

PURPOSE: To evaluate and the long term course of patients with lupus nephritis, METHOD: Thirty seven patients with lupus nephritis followed in a referral, tertiary care center of a developing country (Brazil) were studied. The length of follow up was 52.4 + 13.3 months and mean age was 26.05 + 11.12 years. 84% of the patients were females and class IV nephritis was found to be the most frequent (80%). RESULTS: At the time of renal biopsy mean serum creatinine was 1.74 + 1.15 mg/dl, and 24 h-proteinuria was 2.62 + 2.89 g. Fifty one per cent of the patients with elevated serum creatinine showed a decrease in these values. Of the variables studied (age, sex, proteinuria, presence of hypertension and serum creatinine at biopsy), serum creatinine elevation was the only one to be associated with poorer prognosis. Remission of the nephrotic syndrome occurred in 65% of the patients. Actuarial survival rate was 96% at 1 year, 82% at 5 years, 70% at 10 years and 70% at 12 years. Five patients developed end stage renal failure and 7 died. Infection was the most frequent(57%) cause of death. CONCLUSION: Among several factors studied the only which has been associated with chronic renal failure was elevated serum creatinine at the time of biopsy. Infections were the main cause of death.

Glomerulonefrite lúpica: estudo da evoluçäo a longo prazo / Lupus nephritis: a long term follow-up

OBJETIVO: Estudar a apresentação clínica e a evolução de pacientes portadores de glomerulonefrite lúpica. CASUÍSTICA E MÉTODOS: Foram estudados 37 pacientes portadores de glomerulonefrite lúpica, atendidos pela Disciplina de Nefrologia - Faculdade de Medicina de Botucatu, com seguimento médio de 52,4 + ou - 13,3 meses. Os dados foram obtidos através do levantamento retrospectivo dos prontuários. RESULTADOS: A idade média foi de 26,05 + ou - 11,12 anos, com predomínio do sexo feminino (84 por cento) sendo que a glomerulonefrite classe IV foi a mais freqüente (80 por cento). No início do seguimento a média da creatinina sérica foi de 1,74 + ou - 1,15 mg/dl, e a da proteinúria de 24h foi de 2,62 + ou - 2.89 g. Cinqüenta e um porcento dos pacientes com creatinina sérica elevada apresentaram, durante o seguimento, diminuição desses valores. Dentre diferentes variáveis estudadas, à época da biopsia renal, (idade, sexo, proteinúria, presença de hipertensão arterial e creatinina sérica) a única que se associou com pior prognóstico foi a elevação da creatinina sérica. Remissão da síndrome nefrótica ocorreu em 65 por cento das vezes. A sobrevida atuarial foi de 96 por cento, 82 por cento, 70 por cento e 70 por cento em 1, 5, 10 e 12 anos. Cinco pacientes desenvolveram insuficiência renal crônica terminal e sete morreram, sendo infecção a principal causa de óbito (57 por cento) CONCLUSÃO: Em pacientes com nefropatia lúpica, o aumento da creatinina sérica, à época da biópsia, se associou com o desenvolvimento de insuficiência renal crônica ao fim do seguimento e a principal causa de óbito foi processo infeccioso.

Role of ticlopidine on adriamycin-induced nephropathy.

The effect of ticlopidine on rats with adriamycin nephropathy was observed during 26 weeks. In the ticlopidine-treated nephrotic animals (TNG), proteinuria was less than in the untreated nephrotic animals (NG), but this difference was significant only at week 6 (TNG = 47.27 +/- 16.52 versus NG = 100.08 +/- 13.83 mg/24 h, p < 0.01) and week 26 (TNG = 157.00 +/- 28.73 versus NG = 217.00 +/- 21.73 mg/24 h, p < 0.01) after ADR injection. NG presented severe tubulointerstitial abnormalities with a tubulointerstitial lesion index of 3+. No difference in glomerular lesions was observed among the groups (NG median = 6%, TNG median = 4% and TCG median = 2%). The tubulointerstitial lesion index of TNG was less intense (median = 2+) but not different from those of the control groups (CG median = 1+; TCG median = 0+) nor NG (median = 3+). We concluded that the treatment with ticlopidine produced some partially beneficial effects but did not prevent the development of adriamycin-induced nephropathy.

Effect of allopurinol in the course of adriamycin induced nephropathy.

The role of superoxide in adriamycin-induced nephropathy (single dose; i.v. 3 mg/kg) has been studied by blocking superoxide synthesis through the administration of allopurinol (500 mg/L in drinking water). In Experiment I (EI), allopurinol administration was started 3 days prior to nephropathy induction and continued until day 14. In Experiment II (EII) allopurinol administration was started 2 weeks after nephropathy induction and was maintained until the end of the experiment (26 weeks). Affected glomeruli frequency and tubulointerstitial lesion index (TILI) were determined at Weeks 2 and 4 (EI) and Week 26 (EII). In EI, the 24 h mean proteinuria in the nephrotic control group (NCG-I) differed from that of the treated nephrotic group (TNG-I) at Week 1 (TNG = 33.3 +/- 6.39 mg/24 h; NCG = 59.8 +/- 6.3 mg/24 h; p < 0.05) and 2 (NCG-I = 80.0 +/- 17.5 mg/24 h; TNG-I = 49.1 +/- 8.4 mg/24 h; p < 0.05). No glomerular alterations were observed and TILI medians were not different in both nephrotic groups at week 2 (NCG-I = 1+: TNG = 1+) and 4 (NCG = 4+; TNG = 4+). In EII, NCG-II and TNG-II presented different 24 h proteinuria values only at Week 6, (136.91 +/- 22.23 mg/24 h and 72.66 +/- 10.72 mg/24 h, respectively; p < 0.05). Between nephrotic groups, there was no statistical difference in the median of affected glomeruli (CNG-II = 56%; TNG-II = 48%) and TILI (NCG-II = 8+; TNG-II = 9+). Thus, allopurinol was associated with a transient reduction in proteinuria and it did not alter the progression of the nephropathy.

The hemolytic uremic syndrome as a complication of adriamycin nephropathy.

Rats treated with two injections of adriamycin (week 0 and week 12) developed glomerusclerosis and severe tubulointerstitial lesions as described in the literature. In addition, a number of glomerular alterations were present. These included capillary loop dilation, insudation of eosinophilic material, necrosis, duplication of the glomerular basement membrane, severe mesangiolysis with disruption of the mesangial matrix and segmental double-contours. The renal arterioles and interlobular arteries showed endothelial cell swelling. The subendothelial space was infiltrated by fibrinoid material and there was intensive fibrinoid necrosis of the wall of both arteries and arterioles extending into the glomerular tuft. These alterations were very similar to those observed in the hemolytic uremic syndrome. This observation suggests that the two injections of adriamycin, with a long interval in between them, might induce renal lesions similar to those observed in the hemolytic uremic syndrome.

Amastigotes forms of Trypanosoma cruzi detected in a renal allograft.

Trypanosoma cruzi, the causative agent of Chagas' disease assumes two distinct forms in vertebrate hosts: circulating trypomastigote and tissular amastigote. This latter form infects predominantly the myocardium, smooth and skeletal muscle, and central nervous system. The present work describes for the first time the detection of amastigote forms of T. cruzi in the renal parenchyma of a kidney graft recipient one month after transplantation. The patient was serologically negative for Chagas' disease and received no blood transfusion prior to transplant. The cadaver donor was from an endemic area for Chagas' disease. The recipient developed the acute form of the disease with detection of amastigote forms of T. cruzi in the renal allograft biopsy and circulating trypomastigote forms. The present report demonstrates that T. cruzi can infect the renal parenchyma. This mode of transmission warrants in endemic areas of Chagas' disease.

Acute renal failure: clinical outcome and causes of death.

Acute renal failure (ARF) is a frequent complication in hospitalized patients and is strongly related to increase in mortality. In order to analyze the clinical outcome and the prognostic factors in hospital-acquired ARF, a prospective study was performed. Data from 200 patients with established ARF during the period of January 1987 through July 1990 were collected. The incidence of ARF was 4.9/1000 admissions. Renal ischemia (50%) and nephrotoxic drugs (21%) were the main etiologic factors. The histologic study done in 43 patients showed: acute tubular necrosis (53%), tubular hydropic degeneration (16%), glomerulopathies (16%), and other lesions (15%). Dialysis therapy was performed in 101 patients. The mortality rate was 46.5% and the most important causes of death were: sepsis (38%), respiratory failure (19%), and multiple organ failure (11%). Higher mortality was observed in oliguric patients (62.9%) than nonoliguric (34.5%) (p < 0.05) and in ischemic renal failure (56.7%) when compared to nephrotoxic renal failure (14.7%) (p < 0.05). As primary cause of death was not associated to the acute renal failure, we conclude that acute renal failure is an important marker of the gravity of the underlying disease and not the cause of death.

Acute renal failure in renal allograft recipients and patients with native kidneys.

In order to evaluate the role of underlying disease in the high mortality observed in acute renal failure (ARF) and risk factors related to the development of oliguric ARF in renal allograft recipients, two groups were selected: 34 patients with native kidneys, aged 16 and 57 years, and presenting ischemic ARF caused by cardiovascular collapse, with no signs of infection at the time of diagnosis; and 34 renal allograft recipients who developed ARF immediately after transplantation, without rejection. ARF was defined either as 30% increase of basal plasmatic creatinine in patients with native kidneys or nonnormalization of plasmatic creatinine at day 5 after transplantation in renal allograft recipients; oliguria as diuresis < or = 400 mL/24 h. There were no differences in age, male frequency, oliguria presence and duration, need for dialysis, and infection episodes for renal allograft recipients and patients with native kidneys. The development of sepsis (3% and 41%) and death rate (3% and 44%) were higher in patients with native kidneys (p < 0.01). The renal allograft recipients with both oliguric (n = 18) and nonoliguric (n = 16) ARF were evaluated and no difference was observed in the recipient's age, donor's age, cold ischemia time, time elapsed until plasmatic creatinine normalization, donor's plasmatic creatinine or urea, and mean arterial pressure. No differences were observed between the groups regarding frequency of infection episodes during ARF and frequency of death. In conclusion, renal allograft recipients presented a lower death rate and were less susceptible to sepsis. Cold ischemia time, age, and hemodynamic characteristics of the donor did not affect the development of oliguria.

Insuficiência renal aguda: estudo do quadro clínico e prognóstico / Acute renal failure. Clinical statement study and prognosis

A insuficiência renal aguda orgânica (IRAo) é complicaçao freqüente em pacientes hospitalizados, associando-se a altas taxas de mortalidade. OBJETIVO. Analisar os aspectos clínicos e o quadro anatomopatológico de pacientes portadores de IRAo, bem como determinar fatores de prognóstico. MÉTODOS. Foram estudados, de forma prospectiva, 20O pacientes portadores de IRAo internados durante o período de janeiro de 1987 a julho de 1990. RESULTADOS. A freqüência de IRAo foi de 4,9/1.000 internaçoes. As causas mais comuns foram isquemia renal (50 por cento) e drogas nefrotóxicas (22 por cento). O diagnóstico anatomopatológico realizado em 43 pacientes revelou: necrose tubular aguda (53 por cento); degeneraçao) hidrópica tubular (l6 por cento), glomerulopatias (l6 por cento) e outras lesoes (l5 por cento). Tratamento dialítico foi realizado em 50,5 por cento dos pacientes; as principais indicaçoes foram: uremia (l38 vezes, 67 por cento), hipervolemia (45 vezes, 22 por cento), hiperpotassemia (19 vezes, 9 por cento). A taxa de mortalidade foi de 46,5 por cento, sendo as principais causas de óbito: septicemia (38 por cento), insuficiência respiratória (19 por cento) e falência de múltiplos órgaos (11 por cento). Somente dois pacientes (nos quais o tratamento dialítico foi suspenso) morreram por causas ligadas diretamente à insuficiência renal. Houve maior mortalidade entre pacientes oligúricos (62,9 por cento) do que em pacientes nao oligúricos (34,5 por cento) (p<0,05). Pacientes com IRAo isquêmica apresentaram maior mortalidade (56,7 por cento) do que pacientes com IRAo nefrotóxica (14,7 por cento) (p<0,05). Essas diferenças mantiveram-se quando essa comparaçao foi feita apenas entre os pacientes submetidos a tratamento dialítico. CONCLUSAO. As principais causas de óbito nao foram diretamente relacionadas à IRAo. Desta forma, os dados do presente trabalho sugerem que a IRAo é um importante marcador de gravidade de doença de base, e nao um fator determinante do óbito.

[Acute renal failure. Clinical picture and prognosis]. / Insuficiência renal aguda. Estudo do quadro clínico e prognóstico.

UNLABELLED: Acute renal failure (ARF) is a frequent complication in hospitalized patients, and is strongly related to increase of mortality. PURPOSE: To analyze the clinical outcome and the prognostic factors in hospital acquired AFR. METHOD: A prospective study was performed. Data from 200 patients with established ARF admitted during the period of January, 1987 and July, 1990 were collected. RESULTS: The incidence of ARF was 4.9/1000 admissions. Renal ischemia (50%) and nephrotoxic drugs (21%) were the main etiologic factors. The histologic study done in 43 patients showed: acute tubular necrosis (53%), tubular hydrophic degeneration (16%), glomerulopathies (16%) and other lesions (15%). Dialysis therapy was performed in 101 patients and the main indications were: uremia (67%), hypervolemia (22%) and hyperkalemia (9%). The mortality rate was 46.5% and the most important causes of death were: sepsis (38%), respiratory failure (19%) and multiple organs failure (11%). Treatment withdraw was the cause of death in 2 patients. Higher mortality was observed in oliguric patients (62.9%) than non-oliguric (34.5%) (p < 0.05) and in ischemic renal failure (56.7%) when compared to nephrotoxic renal failure (14.7%) (p < 0.05). This difference was maintained when the comparison was done only between dialyzed patients. CONCLUSION: As primary cause of death was not associated to the acute renal failure, we conclude that acute renal failure is an important marker of the gravity of the underlying disease and not the cause of death.

Effects of dietary protein, angiotensin I converting enzyme inhibition and mesangial overload on the progression of adriamycin-induced nephropathy.

Adriamycin, a commonly used antineoplastic antibiotic, induces glomerular lesions in rats, resulting in persistent proteinuria and glomerulosclerosis. We studied the effects of dietary protein and of an angiotensin I converting enzyme inhibitor on the progression of this nephropathy and the evolution of the histological lesions, as well as mesangial macromolecule flow. Adriamycin nephropathy was induced by injecting a single iv dose of adriamycin (3 mg/kg body weight) into the tail vein of male Wistar rats (weight, 180-200 g). In Experiment I animals with adriamycin-induced nephropathy were fed diets containing 6% (Low-Protein Diet Group = LPDG), 20% (Normal-Protein Diet Group = NPDG) and 40% (High-Protein Diet Group = HPDG) protein and were observed for 30 weeks. In Experiment II the rats with adriamycin nephropathy were divided into 2 groups: ADR, that received adriamycin alone, and ADR-ENA, that received adriamycin plus enalapril, an angiotensin I converting enzyme inhibitor. The animals were sacrificed after a 24-week observation period. Six hours before sacrifice the animals were injected with 131I-ferritin and the amount of 131I-ferritin in the glomeruli was measured. In Experiment III, renal histology was performed 4, 8 and 16 weeks after adriamycin injection. At the end of Experiment I the tubulointerstitial lesion index was 2 for LPDG, 8 for NPDG, and 7.5 for HPDG (P < 0.05); the frequency of glomerulosclerosis was 19 +/- 6.1% in LPDG, 42.6 +/- 6% in NPDG, and 54 +/- 9% in HPDG (P < 0.05); and proteinuria was 61.1 +/- 25 mg/24 h in LPDG, 218.7 +/- 27.5 mg/24 h in NPDG, and 324.5 +/- 64.8 mg/24 h in HPDG (P < 0.05). In Experiment II, at sacrifice, 24-h proteinuria was 189 +/- 16.1 mg in ADR, and 216 +/- 26.1 mg in ADR-ENA (P > 0.05); the tubulointerstitial lesion index was 5 for ADR, and 5 for ADR-ENA (P > 0.05); the frequency of glomerulosclerosis was 40 +/- 5.2% in ADR and 44 +/- 6% in ADR-ENA (P > 0.05); the amount of 131I-ferritin in the mesangium was 214.26 +/- 22.71 cpm/mg protein in ADR and 253.77 +/- 69.72 cpm/mg protein in ADR-ENA (P > 0.05). In Experiment III, sequential histological analysis revealed an acute tubulointerstitial cellular infiltrate at week 4, which was decreased at week 8. Tubular casts and dilatation were first seen at week 8 and increased at week 16 when few glomerular lesions were found.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of dietary protein, angiotensin I converting enzyme inhibition and mesangial overload on the progression of adriamycin-induced nephropathy

Adriamycin, a commonly used antineoplastic antibiotic, induces glomerular lesions in rats, resulting in persistent proteinuria and glomerulosclerosis. We studied the effects of dietary protein and of an angiotensin I converting enzyme inhibitor on the progression of this nephropathy and the evolution of the histological lesions, as well as mesangial macromolecule flow. Adriamycin nephropathy was induced by injecting a singl iv dose of adriamycin (3 mg/kg body weight) into the tail vein of male wistar rats (weight, 180-200 g). In Experiment I animals with adriamycin-induced nephropathy were fed diets containing 6 percent (Low-Protein Diet Group = LPDG), 20 percent (Normal-Protein Diet Group = NPDG) and 40 percent (High-Protein Diet Group = HPDG) protein and were observed for 30 weeks. In Experiment II the rats with adriamycin nephropathy were divide into 2 groups: ADR, that received adriamycin alone, and ADR-ENA, that received adriamycin plus enalapril, an angiotensin I converting enzyme inhibitor. The animals were sacrificed after a 24-week observation period. Six hours before sacrifice the animals were injected with 131I-ferritin and the amount of 131I-ferritin in the glomeruli was measured. In Experiment III, renal histology was performed 4, 8 and 16 weeks after adriamycin injection. At the end of Experiment I the tubulointerstitial lesion index was 2 for LPDG, 8 for NPDG, and 7.5 for HPDG (P,0.05); the frequency of glomerulosclerosis was 19 + or - 6.1 percent in LPDG, 42.6 + or - 6 percent in NPDG, and 54 + or - 9 percent in HPDG (P,0.05); and proteinuria was 61.1 + or - 25 mg/24 h in LPDG, 218.7 + or - 27.5 mg/24 h in NPDG, and 324.5 + or - 64.8 mg/24 h in HPDG (P,0.05). In Experiment II, at sacrifice, 24-h proteinuria was 189 + or - 16.1 mg in ADR, and 216 + or - 26.1 mg in ADR-ENA (P.0.05); the tubulointerstitial lesion index was 5 for ADR, and 5 for ADR-ENA (P.0.05); the frequency of glomerulosclerosis was 40 + or - 5.2 percent in ADR and 44 + or - 6 percent in ADR-ENA (P.0.05); the amount of 131I-ferritin in the mesangium was 214.26 + or - 22.71 cpm/mg protein in ADR and 253.77 + or - 69.72 cpm/mg protein in ADR-ENA (P.0.05). In Experiment III, sequential histological analysis revealed an acute tubulointerstitial cellular infiltrate at week 4, whigh was decreased at week 8. Tubular casts and dilatation were first seen at week 8 and increased at week 16 when few glomerular lesions were found. The results suggest that the tubulointerstitial lesions may play a role in the development of glomerulosclerosis in adriamycin-induced nephropathy

Reduction of urine volume ameliorates adriamycin-induced nephropathy.

1. Adriamycin, a commonly used antineoplastic antibiotic, induces glomerular lesions in rats, resulting in persistent proteinuria and glomerulosclerosis. 2. The effect of urine volume on the progression of adriamycin-induced nephropathy was studied in 70 male Wistar rats (180-200 g) observed for 30 weeks and separated into 4 groups: healthy control group (HCG, N = 10) inoculated i.v. with 1 ml of saline, and nephrotic groups inoculated iv with a single dose of adriamycin of 3 mg/kg body weight. The nephrotic rats were separated into 3 groups (N = 20): nephrotic control group (NCG) receiving only adriamycin; dehydrated nephrotic group (DNG) water deprived for 36 h within each 48-h period, and furosemide nephrotic group (FNG) treated with 12 mg/dl furosemide, and 0.9 g/dl NaCl in the drinking water. 3. The 30-week survival rates of the DNG (100%) and HCG (100%) were significantly higher than those of the NCG (85%) and FNG (55%). 4. The proteinuria observed in the HCG (range, 7.38 +/- 0.7 to 13.6 +/- 1.27 mg/24 h) was significantly lower than that observed for all the nephrotic groups throughout the experiment. The DNG presented significantly less proteinuria (range, 42.71 +/- 6.83 to 140.10 +/- 19.22 mg/24 h) than the NCG (range, 35.32 +/- 7.64 to 250.00 +/- 25.91 mg/24 h) from week 10 on. There was no significant difference between the mean 24-h proteinuria of the NCG (range, 35.32 +/- 7.64 to 250.00 +/- 25.91 mg/24 h) and the FNG (range, 35.82 +/- 7.91 to 221.54 +/- 26.74). 5. The mean frequency of damaged glomeruli was 0.3% +/- 0.3 for HCG, 42% +/- 6% for CNG, 40.8% +/- 8% for DNG, and 47% +/- 14% for FNG. The median value of the tubulointerstitial lesion, evaluated by a semiquantitative method, was 0 in HCG, 10 in CNG, 8.5 in DNG and 9.5 in FNG (P < 0.05 for all groups compared to HCG). 6. The data indicate that reduction of urine volume has a protective effect on adriamycin-induced nephropathy.

Reduction of urine volume ameliorates adriamycin-induced nephropathy

1. Adriamycin, a commonly used antineoplastic antibiotic, induces glomerular lesions in rats, resulting in persistent proteinuria and glomerulosclerosis. 2. The effect of urine volume on the progression of adriamycin-induced nephropathy was studied in 70 male Wistar rats (180-200 g) observed for 30 weeks and separated into 4 groups: healthy control group (HCG, N = 10) inoculated i.v. with 1 ml of saline, and nephrotic groups inoculated iv with a single dose of adriamycin of 3 mg/kg body weight. The nephrotic rats were separated into 3 groups (N = 20): nephrotic control group (NCG) receiving only adriamycin; dehydrated nephrotic group (DNG) water deprived for 36 h within each 48-h period, and furosemide nephrotic group (FNG) treated with 12 mg/dl furosemide, and 0.9 g/dl NaCl in the drinking water. 3. The 30-week survival rates of the DNG (100 per cent ) and HCG (100 per cent ) were significantly higher than those of the NCG (85 per cent ) and FNG (55 per cent ). 4. The proteinuria observed in the HCG (range, 7.38 +/- 0.7 to 13.6 +/- 1.27 mg/24 h) was significantly lower than that observed for all the nephrotic groups throughout the experiment. The DNG presented significantly less proteinuria (range, 42.71 +/- 6.83 to 140.10 +/- 19.22 mg/24 h) than the NCG (range, 35.32 +/- 7.64 to 250.00 +/- 25.91 mg/24 h) from week 10 on. There was no significant difference between the mean 24-h proteinuria of the NCG (range, 35.32 +/- 7.64 to 250.00 +/- 25.91 mg/24 h) and the FNG (range, 35.82 +/- 7.91 to 221.54 +/- 26.74). 5. The mean frequency of damaged glomeruli was 0.3 per cent +/- 0.3 for HCG, 42 per cent +/- 6 per cent for CNG, 40.8 per cent +/- 8 per cent for DNG, and 47 per cent +/- 14 per cent for FNG. The median value of the tubulointerstitial lesion, evaluated by a semiquantitative method, was 0 in HCG, 10 in CNG, 8.5 in DNG and 9.5 in FNG (P < 0.05 for all groups compared to HCG). 6. The data indicate that reduction of urine volume has a protective effect on adriamycin-induced nephropathy

Características clínicas e implicaçöes prognósticas do acometimento renal no mieloma múltiplo / Clinical characteristics and prognosis implications of renal involvement in multiple myeloma

O envolvimento renal no mieloma múltiplo tem sido associado com pior prognóstico destes pacientes. A influência da insuficiência renal no quadro clínico e no prognóstico de portadores de mieloma múltiplo foi estudada, retrospectivamente, em 45 pacientes. Pacientes com insuficiência renal, à primeira visita, apresentaram maior freqüência de perda de peso, proteinúria e hipercalcemia. Entre os pacientes com insuficiência renal, as médias de uricemia e VHS foram maiores e a média do hematócrito foi menor. Näo houve diferença com relaçäo a edema, hipertensäo arterial, fraturas e dores ósseas. A regressäo da insuficiência renal ocorreu em 47% dos casos, o que se deu mais freqüentemente no primeiro mês de seguimento. A média da creatinina foi mais baixa entre os pacientes com insuficiência renal reversível. A mediana da sobrevida foi: pacientes com insuficiência renal: 11 meses; pacientes com funçäo renal normal: 50 meses. Entre os pacientes com insuficiência renal, aqueles que apresentaram recuperaçäo da funçäo renal mostraram uma mediana de sobrevida maior (24 meses) do que aqueles com insuficiência renal irreversível (1 mês). Em conclusäo: o envolvimento renal no mieloma múltiplo é comum e freqüentemente reversível. Pacientes com insuficiência renal tiveram pior prognóstico; entre os pacientes com insuficiência renal, a normalizaçäo da funçäo renal conferiu melhor prognóstico