Saudi Journal of Kidney Diseases and Transplantation

ORIGINAL ARTICLE
Year
: 2004  |  Volume : 15  |  Issue : 4  |  Page : 440--446

Spectrum and Outcome of Primary Glomerulonephritis


Jamal S Al Wakeel, Ahmed H Mitwalli, Nauman Tarif, Awatif A Alam, Durdana Hammad, Hassan Abu-Aisha, Nawaz Memon, Fathia Sulimani, Akram Askar, Abdo Qudsi 
 Department of Medicine, King Khalid University Hospital, Riyadh, Saudi Arabia

Correspondence Address:
Jamal S Al Wakeel
Department of Medicine (38), King Khalid University Hospital, P.O. Box 2925, Riyadh, 11461
Saudi Arabia

Abstract

Glomerulonephritis (GN) is a major cause of chronic renal failure (CRF). To evaluate the trends and outcome with modern improved treatment strategies, we retrospectively reviewed the clinical records of 120 patients with biopsy proven primary GN at our center from January 1990 to June 2001. All the biopsy specimens were subjected to light, electron and immunofluorescent microscopy. The recorded clinical parameters included the presenting symptoms, blood pressure readings, complete blood count, urinalysis, 24-hr urinary protein excretion, creatinine clearance besides rendered therapy and the outcome. Focal segmental glomerulosclerosis was the most common GN and accounted for 56 (47.6%) cases. The frequency of other GN cases in our study included IgA GN in 21 (17.5%) patients, membranous GN in 20 (16.7%), minimal change disease (MCD) in 13 (10.8%), membranoproliferative GN in 4 (3.3%), post infection in 4 (3.3%) and rapidly progressive glomerulonephritis (RPGN) in 2 (1.7%). The type of nephropathy had great influence on outcome and response to therapy. The deterioration of patients with FSGS was the fastest of the glomerulopathies, and nine (16.1%) patients developed end-stage renal failure (ESRD). MCD and post infection GN had the best outcome. Corticosteroids alone along with supportive medication conferred good results in MCD, while combined therapies of mycophenolate mofetil (MMF) and/or cyclophosphamide with corticosteroids provided better outcomes in the rest of the GN. RPGN responded well to the cyclophosphamide and the patients did not develop ESRD. Hyperuricemia, high serum creatinine and hypertension predicted worse outcomes. The control of blood pressure and glucose, and treatment of hyperuricemia and hypoalbuminemia had salutary effect on the outcome. We conclude that due to the better delivered care the outcome of primary GN has improved over the years. However, FSGS is still the most frequently encountered primary GN and has the worst outcome. In the present study, combined therapies with corticosteroids and cytotoxic drugs and supportive therapy were associated with better outcome.



How to cite this article:
Al Wakeel JS, Mitwalli AH, Tarif N, Alam AA, Hammad D, Abu-Aisha H, Memon N, Sulimani F, Askar A, Qudsi A. Spectrum and Outcome of Primary Glomerulonephritis.Saudi J Kidney Dis Transpl 2004;15:440-446


How to cite this URL:
Al Wakeel JS, Mitwalli AH, Tarif N, Alam AA, Hammad D, Abu-Aisha H, Memon N, Sulimani F, Askar A, Qudsi A. Spectrum and Outcome of Primary Glomerulonephritis. Saudi J Kidney Dis Transpl [serial online] 2004 [cited 2020 Feb 22 ];15:440-446
Available from: http://www.sjkdt.org/text.asp?2004/15/4/440/32875


Full Text

 Introduction



Glomerulonephritis (GN) is a major cause of chronic renal failure (CRF) and end-stage renal disease (ESRD) [1] that requires renal replacement therapy, which has great financial burden on any health budget. Therefore, the trends of GN, their racial and geographical variations, and factors contributing to progre­ssive functional deterioration of the renal function must be studied in order to develop better strategies of management of these lesions.

Recently early detection of GN and/or advanced treatment with strict monitoring of blood pressure, diabetes and proteinuria along with supportive medication such as erythro­poietin for anemia, albumin and antioxidant vitamins have changed the outcome of patients with GN.

We aim in this study to describe our expe­riences with primary GN including their presentation, prevalence, trends, course, treat­ment provided and outcome.

 Materials and Methods



We retrospectively reviewed the medical records of 120 patients with biopsy proven primary GN at our center from January 1990 to June 2001. All the biopsy specimens were subjected to light, electron and immunofluo­rescent microscopy. The studied clinical varia­bles included findings such as proteinuria, hematuria, hypertension, edema or infection. The laboratory investigations included serum creatinine, blood urea, 24-hr urinary protein, creatinine clearance, complete urinalysis, urine culture, serum uric acid, triglyceride and chole­sterol, complete blood count, liver function tests and fasting blood sugar. All lab values were recorded at first follow up and 6 monthly thereafter till last follow up.

Therapy intended for the primary GN such as corticosteroids and cytotoxic agents, anti­hypertensives and supportive medications such as erythropoietin, albumin, calcium carbonate, antioxidants and vitamins were reviewed. The antihypertensives included beta-blockers in 46 (38.3%) angiotensin converting enzyme inhibitors (ACEI) in 62 (51.66%), Calcium channel blockers (CCB) in 29 (24.1%) and diuretics in 41 (34%).

Statistical Analysis

Stat pack gold statistical package was used for analysis of the collected data. Values are presented as mean ± Standard error (SE). Regression analysis was used to see the effect of baseline covariates like age, sex, serum creatinine, 24-hr urinary protein, uric acid, hypertension and diabetes on the progression of disease. Student "t" test was done to compare the values and level of significance that was set as P 3 /µL, Na + 138 ± 1.5 mmol/L, K + 5.7 ± 0.3, triglycerides 3.5 ± 1.1 mmol/L, cholesterol 5.9 ±1.4 mmol/L. [Table 1] shows the clinical and laboratory characteristics in patients in each GN found in our study.

[Table 2] shows that 94 (78.3 %) patients received corticosteroids alone, and 20 (16.7%) received steroids along with cytotoxic agents including two patients who received MMF along with steroids, the treatment choice and outcome of the treated patients in our study.

[Table 3] shows that 37 (30.8%) patients dete­riorated, while 83 (69.2%) patients remained stable or improved; 29 (24.1%) patients improved to normal (ie. the levels of serum creatinine, 24-hr urinary protein, creatinine clearance, uric acid and serum albumin and cholesterol as well as blood pressure).

[Table 4] shows that 33 (27.5%) patients had doubling of serum creatinine at last follow­up. Nine FSGS patients, two IgA and one mesangioproliferative nephropathy patients developed ESRD. A life table analysis showed fastest rate of doubling of baseline serum creatinine in FSGS patients [Figure 1]. [Table 5] shows the serum creatinine level during the follow-up period during the first and last visits.

BP was well controlled at last follow-up compared to baseline that there was a 9.1% relative risk reduction in systolic BP and 30% relative risk reduction in diastolic BP . A similar improvement in cholesterol 5.8 ± 0.7 vs 5.1 ± 0.8 mmol/L was observed due to the lipid lowering medication in these patients; 17 patients had serum cholesterol above 6 mmol/L at baseline (normal [2] in 1984 reported the prevalence of FSGS as 22.1%, while Jorgenson et al [3] in 1985 found it to be 7.1%. In 1990, Huraib et al [4] found FSGS to be 11.4%, while Akhtar et al [5] reported it FSGS to be 40.8% in 1996 and 34.6% from to be 34.9% and Mitwalli et al [6],[7] found the central province of Riyadh, Saudi Arabia in 1999. An increasing trend is noted for FSGS in Kingdom of Saudi Arabia. Similar increasing incidence is found to be in some other parts of the world also. [8],[9] Piero et al have found a 10 fold increase in the incidence of FSGS over 20 years period in Europe while Braden et al [10] in 2000 reported a 22.6% increase in the incidence of FSGS over four years in U.S.A. In the present study FSGS was the leading cause of Nephrotic Syndrome and presented with nephrotic range of protei­nuria, hypertension and hematuria. Deterio­ration of renal function was fastest and 20 (21.2%) had doubling of serum creatinine within 3.9 + 0.8602 years and 9 (16.1%) patients went into ESRD.

In our study, the patients with FSGS pro­gressed to ESRD more than other primary GN. However, the total number of patients with renal failure was less in the present study as compared to past studies [10],[11],[12] Furthermore, the patients in the present study who pro­gressed to CRF had high baseline uric acid and serum creatinine at the time of presentation. A similar relationship of high serum crea­tinine with worse outcome was reported by previous studies. [10]

In our study, IgA and mesangioproliferative GN accounted for similar percentage (17%) reported before from Saudi Arabia but smaller percentage of the primary GN in comparison to the far eastern countries like China, Hong Kong and Taiwan, where IgA is the com­monest and predominant GN accounting for 50% of total number of the encountered cases. [13],[14] However, the outcome of this GN was marginally less favorable than the past experience from Saudi Arabia, where 50% of patients developed CRF over 20 years compared to 42% over nine years in our study. [1]

In the present study, the minimal change disease had a favorable outcome, while the patients with post infection GN were quite less in number and all the patients recovered completely with no immunosuppressant. The patients with RPGN in the present study responded well to the steroids and cytotoxic medication and their condition improved and none of them developed ESRD.

Due to the supportive medication in the present study, there was a great overall decrease in the 24-hr urinary protein excretion, with improvement of serum albumin and hemo­globin. Furthermore, we could reduce the level of serum uric acid, triglycerides and cholesterol, and control of BP.

We conclude that due to the better delivered care the outcome of primary GN has improved over the years. However, FSGS is still the most frequently encountered primary GN and has the worst outcome. In the present study, combined therapies of corticosteroids and cytotoxic drugs besides supportive manage­ment were associated with better outcome.

References

1Kumar V, Cotran R, Robbins S. The kidney and its collecting system. In: Basic Pathology, 6th edition (ed), W.B. Saunders Company, 1997; 439-70.
2Qunibi WY, Al-Sibai MB, Taher S, Akhtar M. Renal disease in Saudi Arabia: a study of 147 renal biopsies. King Faisal Specialist Hospital Journal 1984;4:317-23.
3Jorgenson HE, Malik SH, Paul TT, Wohra PC. Renal disease in Saudi Arabia: Ann Saudi Med 1985;5:195.
4Huraib SO, Abu-Aisha H, Mitwalli A, et al. The spectrum of renal disease found by kidney biopsies at King Khalid University Hospital. Saudi Kidney Dis Transplant Bull 1990;1:15-9.
5Akhtar M, Qunibi W, Taher S, et al. Spectrum of renal disease in Saudi Arabia. Ann Saudi Med 1990;10:37-44.
6Mitwalli AH, Al-Wakeel JS, Al-Mohaya SS, et al. Pattern of glomerular disease in Saudi Arabia. Am J Kidney Dis 1996;27 (6):797-802.
7Mitwalli AH, Al Wakeel J, Abu-Aisha H, et al. Prevalence of glomerular disease: King Khalid University Hospital, Saudi Arabia. Saudi J Kidney Dis Transplant 2000;ll(3):442-8.
8Hass M, Spargo BH, Coventry S. Increasing incidence of focal segmental glomerulo­sclerosis among adult nephropathies: a 20­years renal biopsy study. Am J Kidney Dis 1995;26:740-50.
9Barisoni LD, Agati V. The changing epidemiology of focal segmental glomerulo­sclerosis in New York City. Mod Pathol 1994;7:156A.
10Braden GL, Mulhern JG, O'Shea MH, Nash SV, Ucci AA Jr, Germain MJ. Changing incidence of glomerular disease in adults. Am J Kidney Dis 2000;35(5):878-83.
11Shiiki H, Dohi K. Primary focal segmental glomerulosclerosis: clinical course, predictors of renal outcome and treatment. Intern Med 2000;39(8):606-11.
12Matousovic K, Rossmann P, Part V. Focal Segmental Glomeruloscleross. Vintr Lek 1991;37(7-8):633-8.
13Levy M, Berger J. Worldwide perspective of IgA nephropathy. Am J Kidney Dis 1988;12:340-7.
14Li LS. Renal disease in China: overview. Proc 3 rd Asian Pacific C Nephrol, Singapore 1986;292-6.