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 Table of Contents  
Year : 2020  |  Volume : 4  |  Issue : 1  |  Page : 21-24

Corrected estimated glomerular filtration rate is a predictor for survival in multiple myeloma patients

1 Department of Medicine, Tripoli Central Hospital, Tripoli University, Tripoli, Libya
2 Hematology Unit, Tripoli Children Hospital, Tripoli, Libya
3 Department of Oncology, Tripoli Medical Center, Tripoli, Libya
4 Department of Medicine, Tripoli Central Hospital, Tripoli, Libya
5 Medical Student, Tripoli University, Tripoli, Libya
6 Department of Internal Medicine, Alwakar Hospital, Doha, Qatar

Date of Submission07-Feb-2020
Date of Acceptance18-Feb-2020
Date of Web Publication12-Mar-2020

Correspondence Address:
Prof. Elmukhtar Habas
Department of Medical, Tripoli Central Hospital, Tripoli
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/LJMS.LJMS_8_20

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Background/Aim: Kidneys' involvement in multiple myeloma (MM) adversely affects the prognosis. The aim of this study is to assess the relationship between corrected estimated glomerular filtration rate (corrected eGFR) and patients' survival during the first 1 year of follow-up. Methods: Thirty-eight patients with MM and renal impairment followed up from 2013 to 2014 were enrolled in this study. Data were collected and analyzed. Paired t-test and one-way ANOVA were used to compare means at presentation, after 6 months, and at 1 year. Results: There were 20 female (52.6%) and 18 male patients (47.4%) at presentation, aged between 43 and 92 years; their mean weight was 61.3 ± 1.9 kg, and mean body surface area was 1.53 ± 0.04 m2. The mean of blood urea, serum creatinine, and corrected eGFR at presentation was 65.5 ± 7.4 mg/dl, 2 ± 0.41 mg/dl, and 40.6 ± 4.5 ml/min/1.73 m2, respectively. After 6 months, only twenty patients were still alive (i.e., 13 females and 7 males, aged 68.2 ± 2 years), and their mean corrected eGFR was 67.8 ± 29.1 ml/min/1.73 m2. After 1 year, only nine patients (i.e., six females and three males) were alive and continued in follow-up; their mean corrected eGFR was 96.7 ± 10.3 ml/min/1.73 m2. Corrected eGFR mean was statistically significantly lower at presentation than that after 6 months (P = 0.002), whereas during 6 months, the mean corrected eGFR was statistically significantly lower than that after 1 year (P = 0.014), and patients lived a year of follow up, corrected eGFR was higher than at presentation (P = 0.003). The correlation between corrected eGFR and patients' survival at 6 months and 12 months showed that the lower the corrected eGFR, the higher the rate of patient death (P = 0.0001). Conclusion: Corrected eGFR is a good indicator for survival in renal impairment in MM patients during the 1st year of diagnosis.

Keywords: Corrected estimated glomerular filtration rate, multiple myeloma, renal impairment, renal involvement, survival time

How to cite this article:
Habas E, Khamaj A, Rayani A, Aboshala A, Siala I, Tabib M, Habas A, Farfar K, Elzouki IA. Corrected estimated glomerular filtration rate is a predictor for survival in multiple myeloma patients. Libyan J Med Sci 2020;4:21-4

How to cite this URL:
Habas E, Khamaj A, Rayani A, Aboshala A, Siala I, Tabib M, Habas A, Farfar K, Elzouki IA. Corrected estimated glomerular filtration rate is a predictor for survival in multiple myeloma patients. Libyan J Med Sci [serial online] 2020 [cited 2022 Oct 7];4:21-4. Available from: https://www.ljmsonline.com/text.asp?2020/4/1/21/280571

  Introduction Top

Multiple myeloma (MM) was described during the 18th century. It is a plasma cell malignancy and part of hematological disease spectrum ranging from monoclonal gammopathy of unknown significance to plasma cell leukemia. MM is suspected if bone marrow aspiration has ≥10% of clonal plasma cells or bone biopsy-proven plasmacytoma in addition to end-organ damage. Other workers consider that the presence of ≥60% of plasma cells in bone marrow aspiration even without end-organ damage is diagnostic for MM diagnosis.[1] MM is due to an abnormal B-lymphocyte clonal disease of plasma cells, leading to increase of plasma cells in bone marrow and peripheral blood, producing an increase in monoclonal protein synthesis, lytic bone lesions, and renal insufficiency (RI).[2] RI occurs in about 20%–40% of MM at presentation.[2],[3],[4],[5] Creatinine clearance reduced in about 50% of newly diagnosed MM patients. Other studies reported that renal involvement had been detected in 15%–40% of MM patients. Approximately 30%–40% of MM patients had serum creatinine above 1.5 mg/100 ml, and most of the MM patients had serum creatinine <4 mg/dl at diagnosis.[2],[6],[7],[8] Moreover, other studies conducted in different district hospitals reported that about 10% of MM patients presented with severe renal failure that required urgent hemodialysis.[3],[9] Others reported that RI was in 30%–50% when serum creatinine was ≥1.5 mg/dl in MM.[8] Others considered serum creatinine ≥2 mg/dl as the upper limit of normal kidney function, then newly diagnosed MM patients had RI were about 20%.[10],[11],[12]

The etiology of RI in MM is mainly due to monoclonal light chains' toxic effect on different nephron tissues. Amyloidosis, hypercalcemia, dehydration, drugs' toxic effects, and contrast nephropathy are common contributory risk factors for RI in MM. Renal function improves usually after good hydration, correction of hypercalcemia, and discontinuation of nephrotoxic drugs in most of the MM patients who have RI. Half of the MM patients who presented with RI recover during the first 6 weeks of presentation with good hydration. Later, recovery of renal function in MM patients is possible, and even regular long-term hemodialysis may be discontinued in some patients. Those patients who do not recapture the normal renal function will survive with mild or moderate RI. A study reported that only 1% of the MM patients developed end-stage renal disease and required long-term regular hemodialysis.[13]

Normal corrected estimated glomerular filtration rate (eGFR) in a healthy human ranges between 90 and 130 mL/min/1.73 m2. Corrected eGFR affected by gender, muscle mass, and other factors increase or decrease serum creatinine concentration. Corrected eGFR is more precise for renal function assessment than serum creatinine and urea.[12] Although technetium-99–labeled, diethylene-triamine-pentacetic acid; chromium-51–labeled ethylenediaminetetraacetic acid; and 125I-iothalamate are used, inulin is still the accurate method to measure glomerular filtration rate (GFR). In clinical practice, creatinine clearance is commonly used to assess GFR, although creatinine clearance gives higher GFR value by about 5%–10% of the actual GFR.[14],[15]

Cockcroft–Gault and Modification of Diet in Renal Disease study equations are the most accurate used formulae to calculate eGFR in chronic kidney disease (CKD) patients.[16],[17] Other formulas, such as CKD epidemiology collaboration equation, serum cystatin-C, and urinary creatinine were used to calculate eGFR in MM patients. In acute RI, eGFR assessed by the above-mentioned methods was not accurate enough, and the RIFLE and Acute Renal Injury Network criteria are most appropriate to assess RI severity in this situation, although they need to be validated carefully especially in MM patients on chemotherapy.[17]

To our knowledge, there is no study performed to assess the effectiveness of corrected eGFR on the prognosis of MM patients in Libya; therefore, this study was conducted.

  Methods Top

Records of 129 MM patients were studied retrospectively. The patients were followed up in the Medical Department at Tripoli Central Hospital (TCH), Sabrata Oncology Center and Tripoli Medical Center. Out of these 129 patients, 38 patients had raised serum creatinine and urea and low corrected eGFR during a year of follow-up after MM diagnosis. Patients' gender, age, body weight, complete blood picture, blood urea, serum creatinine, and electrolytes were collected from their follow-up notes at presentation, after 6 months, and at 1 year of follow-up during 2013–2014. GFR was calculated by Cockcroft–Gault equation[18] (creatinine clearance value = [140 − age] [weight (kg) × 0.85 if female]/[72 × Scr]), adjusted for individual body surface area (BSA). BSA was calculated by Mosteller method[19] (BSA [m2] = square root of [height (cm) × weight (kg)]/3600). Corrected eGFR was calculated by (corrected eGFR = GFR × 1.73/BSA). The study was approved by the TCH Ethical and Scientific Committee.

Statistical analysis

Statistical analysis was conducted by IBM-SPSS (version 19.0, Chicago, IL, USA). Quantitative data were expressed as mean ± standard deviation and range (minimum, maximum). Paired Student's t-test and one-way ANOVA analysis were used to compare the mean differences of the parameters at presentation, after 6 months, and at 1 year from the diagnosis of MM. P < 0.05 was considered statistically significant.

  Results Top

At the time of presentation of MM with RI, 38 patients' records were diagnosed and reviewed. They were 20 females (52.6%) and 18 males (47.4%). After 6 months of follow-up, twenty patients were alive and continued for follow-up. There were 13 females and 7 males. After 1 year of follow-up, only nine patients (six females and three males) were alive and continued follow-up. [Table 1] shows the demographic features and laboratory findings of these patients at the time of diagnosis and in the follow-up periods. The mean corrected eGFR improved over the time of follow-up; it was statistically significantly higher after 6 months and after 1 year than at presentation (P = 0.002 and P = 0.003, respectively). In addition, corrected eGFR after 6 months was lower than that in the 1-year follow-up period (P = 0.014). There was a statistically significant correlation between corrected eGFR and patients' survival after 6 months and 12 months; the lower the corrected eGFR, the higher the rate of patient death after 6 months and 1 year (P = 0001).
Table 1: Demographic characteristics and laboratory results of multiple myeloma patients with renal impairment at the time of diagnosis, 6 months, and 1 year of follow-up

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  Discussion Top

Worldwide, MM consists of about 1% of the whole malignancies, and it accounts of about 10% of hematologic malignancies.[20],[21] In this study, 129 patients were diagnosed as MM in the main cancer centers in the western part of Libya. Population of this part of Libya was around 60% of the total Libyan population (i.e., around 6 million during the study period). Hence, it can be predicted that MM prevalence was about 3.6/100,000 in the western part of Libya. It was reported that MM was common in men than women, especially in African-Americans compared with Caucasians-Americans.[22] There was a female predominance (2:1) when MM patients were diagnosed at the time of conducting this study.

In this study, RI was reported in about 30% of the MM patients studied (creatinine ≥2 mg/dl), but others reported higher frequency. The difference between this study reported result might be due to the lower serum creatinine used compared by the other previous studies.

Furthermore, in this study, they were 38 patients who had renal involvement by MM at the time of presentation. Eighteen patients died during the first 6 months, 16 of them had corrected eGFR ≤20 ml/min/1.73 m2, and two patients had corrected eGFR ranged from 20 to 25 ml/min/1.73 m2. Of the rest 20 patients, 11 patients had corrected eGFR ≤48 ml/min/1.73 m2 and died during the next 6 months. Only nine patients who had corrected eGFR of 96.68 ml/min/1.73 m2 stayed alive till the end of the 1st year of follow-up after diagnosis. It seems that MM patients who had lower corrected eGFR died earlier.

  Conclusion Top

Corrected eGFR is a significant prognostic indicator for survival in MM patients with renal involvement.


The authors would like to acknowledge the help and assistance of nurses and administrative workers in the hospitals where the enrolled patients were treated.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


The study was conducted when Prof. Elmukhtar Habas worked at Medical Department, Tripoli Central Hospital, Tripoli, Libya.

  References Top

Rajkumar SV. Multiple myeloma: 2013 update on diagnosis, risk-stratification, and management. Am J Hematol 2013;88:226-35.  Back to cited text no. 1
Kyle RA, Gertz MA, Witzig TE, Lust JA, Lacy MQ, Dispenzieri A, et al. Review of 1027 patients with newly diagnosed multiple myeloma. Mayo Clin Proc 2003;78:21-33.  Back to cited text no. 2
Alexanian R, Barlogie B, Dixon D. Renal failure in multiple myeloma. Pathogenesis and prognostic implications. Arch Intern Med 1990;150:1693-5.  Back to cited text no. 3
Bladé J, Fernández-Llama P, Bosch F, Montolíu J, Lens XM, Montoto S, et al. Renal failure in multiple myeloma: Presenting features and predictors of outcome in 94 patients from a single institution. Arch Intern Med 1998;158:1889-93.  Back to cited text no. 4
Eleutherakis-Papaiakovou V, Bamias A, Gika D, Simeonidis A, Pouli A, Anagnostopoulos A, et al. Renal failure in multiple myeloma: Incidence, correlations, and prognostic significance. Leuk Lymphoma 2007;48:337-41.  Back to cited text no. 5
Knudsen LM, Hippe E, Hjorth M, Holmberg E, Westin J. Renal function in newly diagnosed multiple myeloma – A demographic study of 1353 patients. The Nordic Myeloma Study Group. Eur J Haematol 1994;53:207-12.  Back to cited text no. 6
Knudsen LM, Hjorth M, Hippe E. Renal failure in multiple myeloma: Reversibility and impact on the prognosis. Nordic Myeloma Study Group. Eur J Haematol 2000;65:175-81.  Back to cited text no. 7
Terpos E, Katodritou E, Tsiftsakis E, Kastritis E, Christoulas D, Pouli A, et al. Cystatin-C is an independent prognostic factor for survival in multiple myeloma and is reduced by bortezomib administration. Haematologica 2009;94:372-9.  Back to cited text no. 8
Doyle A, Soutar R, Geddes CC. Multiple myeloma in chronic kidney disease. Utility of discretionary screening using serum electrophoresis. Nephron Clin Pract 2009;111:c7-11.  Back to cited text no. 9
Torra R, Blade J, Cases A, Lopez-Pedret J, Montserrat E, Rozman C, et al. Patients with multiple myeloma requiring long-term dialysis: Presenting features response to therapy and outcome in a series of 20 cases. Br J Haematol 1995;91:854-9.  Back to cited text no. 10
Dimopoulos MA, Kastritis E, Rosinol L, Bladé J, Ludwig H. Pathogenesis and treatment of renal failure in multiple myeloma. Leukemia 2008;22:1485-93.  Back to cited text no. 11
Rayner HC, Haynes AP, Thompson JR, Russell N, Fletcher J. Perspectives in multiple myeloma: Survival prognostic factors and disease complications in a single center between 1975 and 1988. Q J Med 1991;79:517-25.  Back to cited text no. 12
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Kooman JP. Estimation of renal function in patients with chronic kidney disease. J Magn Reson Imaging 2009;30:1341-6.  Back to cited text no. 14
Duncan L, Heathcote J, Djurdjev O, Levin A. Screening for renal disease using serum creatinine: Who are we missing? Nephrol Dial Transplant 2001;16:1042-6.  Back to cited text no. 15
Levey AS, Eckardt KU, Tsukamoto Y, Levin A, Coresh J, Rossert J, et al. Definition and classification of chronic kidney disease: A position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int 2005;67:2089-100.  Back to cited text no. 16
International Myeloma Working Group. Criteria for the classification of monoclonal gammopathies, multiple myeloma and related disorders: A report of the International Myeloma Working Group. Br J Haematol 2003;121:749-57.  Back to cited text no. 17
Cockcroft DW, Gault MH. Prediction of creatinine clearance from serum creatinine. Nephron 1976;16:31-41.  Back to cited text no. 18
Mosteller RD. Simplified calculation of body-surface area. N Engl J Med 1987;317:1098.  Back to cited text no. 19
Rajkumar SV. Treatment of multiple myeloma. Nat Rev Clin Oncol 2011;8:479-91.  Back to cited text no. 20
Rajkumar SV, Gahrton G, Bergsagel PL. Approach to the treatment of multiple myeloma: A clash of philosophies. Blood 2011;118:3205-11.  Back to cited text no. 21
Landgren O, Weiss BM. Patterns of monoclonal gammopathy of undetermined significance and multiple myeloma in various ethnic/racial groups: Support for genetic factors in pathogenesis. Leukemia 2009;23:1691-7.  Back to cited text no. 22


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