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NDT Advance Access published online on December 8, 2007
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfm836
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Renal Disease in HIV-Seropositive Patients in Nigeria: an Assessment of Prevalence, Clinical Features and Risk Factors

Chioma Pedro Emem1, Fatiu Arogundade2, Abubakr Sanusi2, Kayode Adelusola3, Friday Wokoma1 and Adewale Akinsola2

1 Department of Medicine, University of Port-Harcout Teaching Hospital, Port-Harcout 2 Renal Unit, Department of Medicine, Obafemi Awolowo University Teaching Hospitals Complex, PMB 5538 Ile-Ife, Osun State, Nigeria 3 Department of Morbid Anatomy and Forensic Medicine, Obafemi Awolowo University Teaching Hospitals Complex, PMB 5538 Ile-Ife, Osun State, Nigeria

Correspondence and offprint requests to: Fatiu A. Arogundade, Renal Unit, Department of Medicine, Obafemi Awolowo University Teaching, Hospitals Complex, P.M.B 5538, Ile-Ife, Osun State, Nigeria; Fax: +234-036-230141; E-mail: fatiu3{at}yahoo.com



   Abstract
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 Abstract
Introduction
 Methodology
 Results
 Discussion
 References
 
In order to determine the pattern of renal disease and risk factors for renal disease in HIV-infected Nigerians, we studied 400 consecutive HIV/AIDS patients (210 males, 190 females) aged between 18 and 65 years (mean ± SD; 34.6 ± 9.4 years), and examined renal disease factors attributable to the infection. Diagnosis of renal disease was based on the consistent presence of at least 1+ albuminuria and/or elevated serum creatinine (>132 µmol/l) as well as the absence of other identifiable causes of chronic kidney disease (CKD). We determined socio-demography and clinical findings, as well as full laboratory work-ups including haemogram, CD4+ cell count, serum electrolytes, urea, creatinine, protein, cholesterol and urine analysis. Renal biopsies were taken in 10 patients who had moderate to massive proteinuria and had consented to the procedure. Finally, we compared HIV/AIDS cases with and without renal disease to determine the risk factors for nephropathy. We observed a high prevalence of renal disease (proteinuria and/or elevated serum creatinine), which was present in 152 (38%) of the patients. This subgroup included 74 males and 78 females with a M:F ratio of 1:1. The mean age (±SD) was 35.8 (±10.01) years. Systolic and/or diastolic hypertension was seen in 13.2% of these patients while the mean (± SD) body mass index (BMI) and packed cell volume (PCV) were 18.5 (±3.1) kg/m2 and 25.26 (±6.81)%, respectively. The mean (±SD) CD4+ count was 246.49 (±192.8) cells/µl, while the mean (±SD) serum creatinine and 24-h urine protein excretion rates were 210.11 (±337.8) µmol/l and 2.57 (± 2.42) g/day, respectively. In subjects with and without nephropathy, there were significant differences in age, BMI, serum cholesterol, serum albumin and CD4+ counts, suggesting that these parameters may be risk factors for nephropathy. Histology revealed mainly focal glomerulosclerosis (FGS) with glomerular collapse. We conclude that the prevalence of proteinuria in HIV-seropositive patients is high in Nigeria. Such subjects show an equal male:female distribution, and glomerular histology revealed that a majority of biopsied patients had the collapsing FSGS variant. The risk factors for renal disease included severity of the HIV infection (inferred from the generally low CD4+ count), anaemia, malnutrition and increasing age.

Keywords: Blacks; nephropathy; prevalence; proteinuria; risk factors



   Introduction
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 Abstract
 Introduction
Methodology
 Results
 Discussion
 References
 
Renal syndromes in HIV-infected patients may manifest as acute renal failure (ARF) or chronic renal failure (CRF) [1–5]. HIV-associated nephropathy (HIVAN) is said to be present when a seropositive patient presents with persistent proteinuria, progressively worsening azotemia with preservation of normal kidney size or even enlarged kidneys, and renal histological findings of focal segmental glomerulosclerosis (FSGS) upon biopsy. In addition, these patients usually have relatively normal blood pressure and rapid progression to renal failure and end-stage renal disease (ESRD). Additional glomerulopathies documented in HIV or AIDS patients include immune complex disease (ICD), mesangial proliferative GN, membranous GN or thrombotic microangiopathies and other pathologies. However, classic HIV-associated nephropathy with focal glomerulosclerosis is the most common disorder [6,7]. It occurs in 3–10% of HIV-infected individuals and is at a high prevalence in black males with low socio-economic status [8]. It is also the third leading cause of ESRD among African Americans aged 20–64 years and is an important risk factor for ESRD [8,9].

In Nigeria over the last decade, there has been an exponential increase in the prevalence of HIV, from less than 1% to 5.8% (range 2–15% in different communities in different states) [10].

Chronic renal failure is highly prevalent in Nigeria; it accounts for 8–12% of hospital admissions, and has an estimated prevalence of about 300–400 per million [11,12]. The common causes are hypertension, chronic glomerulonephritis and Type 2 Diabetes Mellitus (DM) [13].

Because there is growing concern that HIV is contributing significantly to the increasing prevalence of CRF, an appraisal of this interaction is warranted. This study therefore aimed to determine the prevalence, clinical features, and risk factors for renal disease in HIV-positive Nigerians.



   Methodology
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 Abstract
 Introduction
 Methodology
Results
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 References
 
The study was carried out among outpatients attending the HIV/AIDS clinic at the Obafemi Awolowo University Teaching Hospital Ile-Ife and the University of Port-Harcout Teaching Hospital, Port Harcout; both centres are situated in the Southern portion of Nigeria.

Four hundred consecutive HIV/AIDS patients who consented to participate in the study were screened for renal disease using standard clinical and laboratory criteria.

Patients were defined as having renal disease if they persistently had either of the following:

1. 1+ albuminuria on at least two occasions (4 weeks apart) and/or
2. serum creatinine above 132 µmol/l (1.5 mg/dl).

Patients with febrile illnesses, DM, hypertension, obstructive uropathy, urinary tract infection and clinical features of glomerulonephritis (GN) preceding HIV seropositivity were excluded from the study. Other exclusion criteria included hepatitis B surface antigen (HBsAg) positivity and presence of antibodies to hepatitis C virus (HCV). The study was approved by the ethics committee of our hospital.

We documented socio-demographic data, clinical findings and anthropometric measurements of the recruited patients. Following this, laboratory work-ups were performed, which included full blood count (FBC), erythrocyte sedimentation rate (ESR), CD4+ count, 24-h urine protein, Na+ and K+. In addition, serum electrolytes (Na+, K+), urea, creatinine, serum proteins and total cholesterol were evaluated. Hypertension was diagnosed in those with systolic and/or diastolic blood pressures of ≥140 mmHg and ≥90 mmHg, respectively, while hypotension was diagnosed in those with systolic and/or diastolic blood pressures of <90 mmHg and <60 mmHg, respectively.

Renal biopsy was offered to all patients with established renal disease with moderate to massive proteinuria (urine protein >2 g/day) but with serum creatinine <250 µmol/l. It was required that these patients should not be clinically uraemic and that they give written informed consent. Spring-loaded Tru-cut biopsy needles were used and the obtained tissues were sent for histology. Following this, we compared all HIV/AIDS patients with renal dysfunction with those having normal function in order to determine risk factors for nephropathy.

Statistical analysis was performed using SPSS version 10.0. The data are expressed using descriptive statistics and percentages. Chi-square analysis and Fisher's exact tests were used for discrete data. Student t-tests and Mann–Whitney U-tests for non-parametric data were used to compare groups. Spearman's correlation coefficients were used to establish associations, and multiple regression analysis was used to evaluate the contributions of the different variables to the observed significance. P-values of <0.05 were taken as statistically significant.



   Results
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 Abstract
 Introduction
 Methodology
 Results
Discussion
 References
 
Socio-demographic characteristics of all recruited patients
Of the 400 patients, 210 (52.5%) were females and 190 (47.5%) were males; the male:female (M:F) ratio was 1.0 : 1.1. Patient age ranged from 18 to 65 years (mean ± SD; 34.6 ± 9.4 years). Of the entire group, 207 (51.75%) were married while 127 (31.75%) were single (Table 1). All of the patients studied were heterosexuals and none had history of intravenous drug use (IVDU). Only 90 patients (22.5%) from the entire study population were on antiretroviral therapy [not highly active anti-retroviral therapy (HAART)] and adherence was poor. Of these 90 patients, 28 (31.1%) had renal disease and 62 (68.9%) were free of renal disease (X2 value = 2.339, P = 0.126).


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  		Table 1. Comparison of socio-demographic and laboratory features between HIV patients with and without renal dysfunction

 
Clinical characteristics of subjects with renal disease
One hundred and fifty-two (38%) of the patients had proteinuria and/or elevated serum creatinine. Of this group, 78 (51.3%) were females and 74 (48.7%) were males, with a M:F ratio of 1.0 : 1.1. Ages ranged from 19 to 65 years (mean ± SD; 35.80 ± 10.01 years) (Table 1).

Fifty (12.5%) were single, 78 (19.5%) married, 8 (2%) divorced and 16 (4%) widowed. Four (1%) of the patients had no formal education, 44 (11%) had primary education, 78 (19.5%) had secondary education while the remaining 26 (6.5%) had post-secondary education (Table 1).

The presence of renal disease was highest in the 30- to –39-year age group which had 57 affected patients (14.25% of the study population), followed by the 19- to 29-year group (42 patients corresponding to 10.5%) and by the 40- to –49-year group (38 patients corresponding to 9.5%). Only 15 (3.75% of the study population) of the patients with renal disease were in the 50- to 65-year age range.

The major clinical problems in patients with renal disease at presentation were vomiting, frothiness of urine and body swelling, which were found in 32.9%, 25% and 23.6% of the patients, respectively. Systolic BPs ranged from 70 to 220 mmHg (mean ± SD; 115.43 ± 21.81 mmHg) while diastolic BPs ranged from 50 to 120 mmHg (mean ± SD; 75.02 ± 12.84 mmHg). Twenty (13.2%) of the patients had hypertension while 22 (14.5%) had hypotension.

BMIs of the patients ranged from 11.6 to 28.6 kg/m2 (mean ± SD; 18.5 ± 3.1 kg/m2). Ninety patients (59.2%) had a BMI <19.0 kg/m2 while only 5 (3.3%) had a BMI >25.0 kg/m2. In the remaining 57 (37.5%) patients, BMIs ranged from 19 to 25 kg/m2.

Dipstick positive proteinuria was 1+ in 82 (20.5%) patients, 2+ in 39 (9.8%), 3+ in 17 (4.3%) and 4+ in 14 (3.5%) patients. Urine microscopy revealed red blood cells in only 4 (2.6%) of the patients while waxy casts were found in 3 (1.9%) of the patients.

The means ± SD of serum creatinine, endogenous creatinine clearance and 24-h urinary protein excretion were 210 ± 337.8 µmol/l (range: 41– 2210 µmol/l), 64.69 ± 38.52 ml/min (range: 4.5–171.7 ml/min) and 2.52 ± 2.42 g/day (range: 1.0–11.2 g/day), respectively. Glomerular filtration rates (GFR) were <60 ml/min in 52.6%, while 8.8% were in ESRD with creatinine clearances <15 ml/min. We also found that 21 out of 96 patients who completed 24-h urine analysis (21.9%) had nephrotic range proteinuria. There was hyponatraemia (serum sodium <130 mmmol/l) in 74.1% of the patients, while only 11.1% had hypokalaemia (serum potassium <3.0 mmol/l). Hyperkalaemia (serum potassium >5.0 mmol/l) was observed in only 5.6%. Means (±SD) for serum albumin and total cholesterol were 34.87 (±6.56) g/l (range = 18–49 g/l) and 3.56 (±0.73) mmol/l (range = 1.6–4.8mmol/l), respectively. Hypoalbuminaemia was found in 45.5% of the patients, while none had hyperlipidaemia despite nephrotic range proteinuria in some of the subjects. The mean (±SD) packed cell volume (PCV) in study subjects was 25.26% (±6.81); actual values ranged between 10 and 45%. PCV was <30 in 69.7% and between 30 and 36% in 24.6%, while only 6.2% of the patients had PCV above 36% (>36–45%).

There was a positive correlation between the degree of proteinuria and serum creatinine (correlation coefficient ‘r’ = 0.444, P = 0.000) (Figure 1), whereas proteinuria was negatively correlated with BMI (r = 0.176; P = 0.000), creatinine clearance (r = 0.450; P = 0.000), PCV (r = 0.326; P = 0.000), CD4 count (r = 0.156; P = 0.019) and serum albumin (r = 0.502; P = 0.000). However, multiple regression analysis controlling for degree of renal function (creatinine clearance) revealed that only proteinuria, serum albumin and packed cell volume were correlated with beta (‘ß’) values of 0.539, 0.532 and 0.355, respectively.


Figure 1
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  		Fig. 1. Correlation between creatinine clearance and proteinuria (r = 0.450, P = 0.000).

 
Assessment of risk factors for renal disease
While assessing risk factors for renal disease, we found that age, body mass index, packed cell volume and CD4 count were significantly different between HIV patients with and without renal dysfunction. Serum albumin and total cholesterol were significantly lower in proteinuric HIV patients than in controls while serum globulin was higher in the proteinuric patients (Table 1). There were no gender differences, as 37.1% (78 out of 210) of females in the study population had renal disease while the corresponding value for males was 38.9% (74 out of 190) (X2 value = 0.062, P = 0.804).

Histological characteristics of biopsied subjects
Histology specimens from 10 patients revealed that 7 had focal segmental glomerulosclerosis with partially collapsed glomeruli, microcystic tubular dilatation with casts and mononuclear cell infiltration (Table 2). The remaining three patients had normal appearance upon light microscopy.


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  		Table 2. Histological findings in biopsied HIV patients with proteinuria (light microscopy)

 


   Discussion
Top
 Abstract
 Introduction
 Methodology
 Results
 Discussion
References
 
In our study, the prevalence of renal disease (determined by proteinuria and/or raised serum creatinine) in HIV/AIDS patients was 38%, which is higher than in the earlier reported studies by Winston et al. [8] and Szczech et al. [14]. Our high prevalence may be due to our entirely Black population, a racial group known to have a high predisposition for HIVAN and other renal diseases. However, our rate of 38% may be higher than the true prevalence of HIVAN since our renal biopsy rates were low. The mean age of patients with renal disease in our study was very similar to those with HIVAN found in other studies, possibly because this is the peak period of sexual activity [14,15]. In contrast to the very high preponderance of male HIVAN reported by some authors, the M:F ratio in our study was nearly 1:1. This is mainly because of the heterosexual mode of transmission in our country that has been documented by other authors [15]. Intra-venous drug use (IVDU) is rare and homosexuality is uncommon in our region [15].

The common clinical findings in our patients were vomiting, frothiness of urine, peripheral oedema and hypertension, all of which reflected the advanced nature of their renal disease even at presentation. The high prevalence of malnutrition adjudged by the low BMI, hypoalbuminaemia, hypocholesterolaemia and anaemia provided further evidence of advanced renal disease. Malnutrition may also be due to impaired oral intake, malabsorption and/or altered metabolism as well as the wasting syndrome that characterizes HIV infection [16]. In agreement with previous work, we found that a large proportion of our patients had anaemia, which further indicated the advanced nature of the infection and renal disease [17,18]. Anaemia in HIVAN patients has been shown to vary depending on the stage of the disease, the CD4+ count and level of renal function [17,18].

In keeping with the observations by various authors that low CD4 counts are a risk factor for nephropathy in HIV/AIDS patients [14,19], we found significantly lower CD4+ counts in subjects with nephropathy than in those without the disease. We also observed that nephropathy patients more frequently had counts of <200 cells/µl, which is in agreement with previous findings [14,19].

The percentage of patients in ESRD in our study was high, which indicates that HIV-related renal disease may be an emerging cause of ESRD in our region. This finding corroborates the report of Winston et al. [8] and the USRDS (1992–1999) data showing that HIVAN is a leading cause of ESRD [8,9]. We also had a high percentage of patients (21.9%) with nephrotic range proteinuria that is the characteristic of HIV-FSGS [3,6,20].

Our finding of varying electrolyte derangements in our subjects is in agreement with previous reports [21–23]. These alterations may be due to renal tubular dysfunction and volume depletion from gastrointestinal losses and excessive insensible loss of sweat secondary to high fever or tropical weather [21—26]. Other documented contributory factors include poor intake, SIADH, use of ketoconazole, amphothericin B and trimethoprim sulfamethoxazole, as well as primary or secondary adrenal insufficiency [21–26].

Our observed significant negative correlation between proteinuria and creatinine clearance further confirmed proteinuria as a major risk factor for renal disease, and a worsening of proteinuria with the degree of dysfunction has been documented by others [27].

A majority of our biopsied patients had collapsing focal segmental glomerulosclerosis, microcystic dilatation and tubular casts, and this agrees with the reports of Pantanowitz et al. [28]. and Han et al. [29], who found that 60% and 83% of their patients, respectively, had FSGS. However, Gerntholtz et al. [30] and Van Der Reijden et al. [31] reported lower figures. Mark et al. [32], in a recent report, found HIV-related immune complex glomerulonephritis with lupus-like features in 18% of their HIV subjects, which is similar to the 21% reported by Gerntholtz et al. [30]. Our study was limited by a lack of immunoflorescence and electron microscopic studies, making it impossible to assess immune complex glomerulonephritis.

In conclusion, proteinuria and elevated serum creatinine occurs in a high proportion of HIV-infected Nigerian patients. These findings may reflect the background of high prevalence of renal disease in this region. A majority of the patients were in the albuminuric stage and were therefore amenable to specific treatment with angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) therapy. A significant proportion (8.8%) had reached ESRD, suggesting that HIVAN may represent an important risk factor for ESRD in our population, and its contribution to the burden and magnitude of ESRD in our country will very likely overwhelm our health system.

In HIV patients, features such as hypertension, malnutrition and peripheral oedema occur frequently, and these may be secondary to the advanced nature of HIV infection and renal disease. The severity of HIV infection, as reflected by the CD4 count and malnutrition, appears to promote the development of nephropathy in our HIV/AIDS population. Hence, efforts geared towards improving nutritional status and drug therapy, particularly the use of HAART, should stem the tide of HIVAN in our population.

In Nigeria, there is a need to provide a renal replacement therapy (RRT) outlet for treatment of the ESRD that results from HIVAN. Up to now, this had been very limited in our region. There is also the need to conduct a nationwide clinico-pathologic study using immunoflourescence and possibly electron microscopy in order to determine the true prevalence of HIVAN in Nigeria.

Conflict of interest statement. None declared.



   References
Top
 Abstract
 Introduction
 Methodology
 Results
 Discussion
 References
 

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Received for publication: 18. 9.07
Accepted in revised form: 25.10.07


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C. I. Esezobor, E. Iroha, E. Onifade, A. O. Akinsulie, E. O. Temiye, and C. Ezeaka
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