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 Table of Contents  
ORIGINAL ARTICLE
Year : 2013  |  Volume : 10  |  Issue : 1  |  Page : 18-21

Hypertension and renal function deterioration in black Africans with autosomal polycystic kidney disease


1 Department of Internal Medicine and Nephrology, Faculty of Health Sciences, University Gaston Berger of Saint-Louis, Saint-Louis, Senegal
2 Department of Nephrology, University Hospital Aristide Le Dantec, Dakar, Senegal
3 Dialysis Unit, ABC Polyclinic, Dakar, Senegal

Date of Web Publication21-Sep-2013

Correspondence Address:
Sidy M Seck
Faculty of Health Sciences, University Gaston Berger of Saint-Louis, Route de Ngallèle, BP: 234, Saint-Louis
Senegal
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Source of Support: None, Conflict of Interest: None


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  Abstract 

Background: High blood pressure (HBP) is a leading cause of end-stage renal disease (ESRD) in black African populations and it is frequently associated with autosomal polycystic kidney disease (ADPKD). We assessed the impact of HBP on progression of renal disease in black Africans with ADPKD.
Objectives and Methods: We performed a retrospective study between 1995 and 2010 in nephrology out-patient clinic. ADPKD was diagnosed according to recent unified criteria add reference and seventh Joint National Committee classification was used for HBP definition. Statistical analyzes were performed with Stata 12 (Statacorp LP, TX, USA).
Results: We included 71 patients (39 males and 32 females) with a mean age of 47±5 years. Prevalence of hypertension was 71.8% and it was present at diagnosis of ADPKD in 48 patients (67.6%). Median delay between HBP and ADPKD diagnosis was 25.6 months. Mean systolic/diastolic blood pressure was 168±30/96±16 mm Hg. After median follow-up of 1823 days, adjusted incidence rate of ESRD in hypertensive and normotensive patients was respectively 0.05 events/100,000 patient-years and 0.03 events/100,000 patient-years (P=0.02). Anti-hypertensive therapy included angiotensin-converting-enzyme (ACE) inhibitors in 51% of patients, but less than 1/3 normalized their blood pressure. At univariate analysis, ESRD was correlated with age, gender, body mass index, HBP and proteinuria. Multiple logistic regression analysis identified age (odds ratio (OR)=1.14; P=0.06) and HBP (OR=1.67; P=0.02) as associated with ESRD.
Conclusion: Hypertension with organ damage is frequent in black African patients with ADPKD. Age and HBP at diagnosis were the main factors associated with ESRD.

Keywords: Black Africans, hypertension, polycystic kidney disease, renal function


How to cite this article:
Seck SM, Cisse MM, Serigne G, Dahaba M, Ka EF. Hypertension and renal function deterioration in black Africans with autosomal polycystic kidney disease. Nig J Cardiol 2013;10:18-21

How to cite this URL:
Seck SM, Cisse MM, Serigne G, Dahaba M, Ka EF. Hypertension and renal function deterioration in black Africans with autosomal polycystic kidney disease. Nig J Cardiol [serial online] 2013 [cited 2022 Sep 26];10:18-21. Available from: https://www.nigjcardiol.org/text.asp?2013/10/1/18/118575


  Introduction Top


Autosomal polycystic kidney disease (ADPKD) is the most common hereditary renal disease in all populations, but data are scarce in black African patients. [1],[2] High blood pressure (HBP) is a leading cause of end-stage renal disease (ESRD) in this population and is frequently associated to ADPKD. [3],[4] This relation is complex as HBP may appear early in ADPKD patients prior to impairment of glomerular filtration rate (GFR) [5],[6] or later at ESRD. Studies from European and American patients had demonstrated that the presence of HBP can worsen the cardiovascular and renal outcomes in ADPKD patients. [7],[8] However, this hypothesis has not yet been confirmed in other populations. The present study was aimed to describe the prevalence and impact of HBP on renal function deterioration in black Africans with ADPKD.


  Materials and Methods Top


We conducted a retrospective study including ADPKD patients followed at our nephrology out-patient clinic between 1995 and 2010. Socio-demographic and clinical data were collected from medical records regularly and these were updated at each visit. All diagnosis of ADPKD was reviewed according to recent unified criteria. [9] Blood pressure (BP) was measured during visits with a validated semi-automatic device. HBP was stratified according to seventh Joint National Committee report [10] and GFR was estimated using four-variables equation from Modification of Diet in Renal Disease (MDRD) study. [11] Patients with incomplete records and those who did not meet ADPKD criteria were not included in the study. Statistical analyzes were performed with Stata version 12 (Statacorp LP, TX, USA). Patients were divided into two groups according to their blood pressure at the first visit (diagnosis). Data were expressed as mean±standard deviation for continuous variables or percentage for categorical variables. For comparison of means, we used Mann-Whitney or Student T-test as appropriate. Incidence rates of ESRD were calculated and Kaplan-Meier analysis was used to compare the occurrence of ESRD with time between hypertensive and normotensive patients.


  Results Top


We included 71 patients (39 males and 32 females) with a mean age of 47±5 years. Hypertension was found in 51 patients (prevalence of 71.8%) and it was present at diagnosis of ADPKD in 48 of them (67.6%). Median delay between HBP and ADPKD diagnosis was 25.6 months (interquartile range of 15 months). Distribution of baseline (first visit) blood pressure levels in patients are presented in [Figure 1]. Mean serum creatinine and estimated GFR at the first visit were 1.75±1.4 mg/dL and 89.7±13.4 mL/min respectively (small skewness). Baseline clinical findings in hypertensive and normotensive patients are presented in [Table 1].
Figure 1: Kaplan-Meier survival curves in patients with and without hypertension at baseline (first diagnosis visit). Compared to normotensives, patients with hypertension at baseline present a significantly more rapid deterioration of their renal function (event=endstage renal disease)

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Table 1: Clinical and biological parameters in hypertensive and normotensive patients at baseline (first diagnosis visit)

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After a median follow-up of 1,832 days (interquartile range of 1188 days), adjusted incidence rate of ESRD was significantly higher in hypertensive versus normotensive patients (respectively 0.05 events/100,000 patient-years vs. 0.03 events/100,000 patient-years, P=0.02). After univariate and multiple logistic regression analyzes, HBP and age were the only risk factors associated to ESRD [Table 2]. Kaplan-Meier survival analysis showed that patients in the HBP group reached more rapidly the end-point that was ESRD [Figure 1].
Table 2: Univariate and multivariate (logistic regression) analyzes for risk factors of end-stage renal disease (GFR<15 ml/min)*

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Anti-hypertensive therapy for the majority of patients comprised ACE inhibitors alone (25 patients) or combined with calcium channel blockers (20 patients). Despite this, blood pressure was not controlled (<140/90 mm Hg) in 56 of them (71.8%). All-cause mortality rate was comparable in hypertensive and normotensive patients at admission (25% vs. 21.7%, P=0.33).


  Discussion Top


Polycystic kidney disease is a probably under-diagnosed disease in Africa with an estimated prevalence of 0.2% in Senegalese patients 2. High prevalence of HBP at diagnosis of ADPKD is compatible with what has been found in previous studies where HBP concerned 50-75% of ADPKD patients. [3],[4],[6],[12] In the majority of patients (around 60%), the rise in BP precedes renal function decline many years before [13] and its prevalence increases with age as cyst volume growth induce GFR decline. [14],[15] Furthermore in ADPKD patients, HBP is a strong determinant for progression to renal function decline. [16] In this study, ADPKD patients with HBP at baseline diagnosis presented an excess ESRD risk of 66% compared to those with normal blood pressure. The high incidence rate of ESRD in our patients can be related to genetic factors specific to African people as it was recently demonstrated in patients with chronic kidney disease (CKD) not related to ADPKD. [17] Genetic mutation located on polycystic kidney disease-1 (PKD-1 gene) was reported in Senegalese patients and these types of mutations are also associated with faster progression to ESRD. [4],[18] Contrasting with data from longitudinal cohorts, larger kidney size did not predict faster progression to ESRD, but this result was probably due to imprecise appreciation of kidney volume in the absence of magnetic resonance imaging. [7] Other factors such as male gender, [16] albuminuria, [16],[19] urinary tract infections, [19] have been associated with renal function decline in ADPKD patients, but significant correlations were not found in our study. Furthermore, patients with a hypertensive ascendant are at higher risk to develop ESRD earlier in their life. [4] Many dietary and pharmacological interventions targeting to control blood pressure in ADPKD patients failed to demonstrate any consistent benefits in slowing GFR decline. [20] Despite the use of anti-hypertensive therapy in our patients, BP was normalized in only 30% of them. Such poor BP control increases risk for proteinuria, ESRD, left ventricular hypertrophy and cardiovascular events. [4]

Early detection and treatment of HBP in ADPKD patients could help reduce the incidence of ESRD [20],[21] and cardiovascular complications, which are the main causes of death in the post-dialysis era. [14],[22] Superiority of an anti-hypertensive class in ADPKD is not clearly demonstrated. Blockers of renin-angiotensin system can efficiently help control blood pressure in ADPKD patients, regression of cardiac hypertrophy [14] and might also reduce cyst progression and GFR decline. [23] Because of this hypothetical benefit, ACE inhibitors were widely prescribed in our patients.


  Conclusion Top


Our study shows that hypertension is frequent in black African patients with ADPKD and usually present when the renal disease is diagnosed. Like in non-black populations, it is strongly associated with a renal function decline in our patients. In the absence of clear evidence about benefit of early HBP detection and treatment, large intervention studies are urgently needed in ADPKD patients living sub-Saharan Africa.

 
  References Top

1.Torres VE, Harris PC, Pirson Y. Autosomal dominant polycystic kidney disease. Lancet 2007;369:1287-301.  Back to cited text no. 1
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2.Fary Ka E, Seck SM, Niang A, Cisse MM, Diouf B. Patterns of autosomal dominant polycystic kidney diseases in black Africans. Saudi J Kidney Dis Transpl 2010;21:81-6.  Back to cited text no. 2
    
3.Gabow PA, Chapman AB, Johnson AM, Tangel DJ, Duley IT, Kaehny WD, et al. Renal structure and hypertension in autosomal dominant polycystic kidney disease. Kidney Int 1990;38:1177-80.  Back to cited text no. 3
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4.Chapman AB, Stepniakowski K, Rahbari-Oskoui F. Hypertension in autosomal dominant polycystic kidney disease. Adv Chronic Kidney Dis 2010;17:153-63.  Back to cited text no. 4
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5.Kelleher CL, McFann KK, Johnson AM, Schrier RW. Characteristics of hypertension in young adults with autosomal dominant polycystic kidney disease compared with the general U.S. population. Am J Hypertens 2004;17:1029-34.  Back to cited text no. 5
    
6.De Almeida EA, Prata MM. Hypertension in autosomal dominant polycystic kidney disease: Observational study in 207 patients with a mean follow-up of 107 months. Rev Port Cardiol 2007;26:1173-82.  Back to cited text no. 6
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7.Torres VE, King BF, Chapman AB, Brummer ME, Bae KT, Glockner JF, et al. Magnetic resonance measurements of renal blood flow and disease progression in autosomal dominant polycystic kidney disease. Clin J Am Soc Nephrol 2007;2:112-20.  Back to cited text no. 7
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8.Gabow PA, Johnson AM, Kaehny WD, Kimberling WJ, Lezotte DC, Duley IT, et al. Factors affecting the progression of renal disease in autosomal-dominant polycystic kidney disease. Kidney Int 1992;41:1311-9.  Back to cited text no. 8
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9.Pei Y, Obaji J, Dupuis A, Paterson AD, Magistroni R, Dicks E, et al. Unified criteria for ultrasonographic diagnosis of ADPKD. J Am Soc Nephrol 2009;20:205-12.  Back to cited text no. 9
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10.Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, et al. Seventh report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure. Hypertension 2003;42:1206-52.  Back to cited text no. 10
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11.Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth D. A more accurate method to estimate glomerular filtration rate from serum creatinine: A new prediction equation. Modification of diet in renal disease study group. Ann Intern Med 1999;130:461-70.  Back to cited text no. 11
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12.Kazancioglu R, Ecder T, Altintepe L, Altiparmak MR, Tuglular S, Uyanik A, et al. Demographic and clinical characteristics of patients with autosomal dominant polycystic kidney disease: A multicenter experience. Nephron Clin Pract 2011;117:c270-5.  Back to cited text no. 12
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13.Ecder T, Schrier RW. Cardiovascular abnormalities in autosomal-dominant polycystic kidney disease. Nat Rev Nephrol 2009;5:221-8.  Back to cited text no. 13
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14.Schrier RW. Renal volume, renin-angiotensin-aldosterone system, hypertension, and left ventricular hypertrophy in patients with autosomal dominant polycystic kidney disease. J Am Soc Nephrol 2009;20:1888-93.  Back to cited text no. 14
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15.Seeman T, Dusek J, Vondrichová H, Kyncl M, John U, Misselwitz J, et al. Ambulatory blood pressure correlates with renal volume and number of renal cysts in children with autosomal dominant polycystic kidney disease. Blood Press Monit 2003;8:107-10.  Back to cited text no. 15
    
16.Grantham JJ. Mechanisms of progression in autosomal dominant polycystic kidney disease. Kidney Int Suppl 1997;63:S93-7.  Back to cited text no. 16
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17.Kopp JB, Nelson GW, Sampath K, Johnson RC, Genovese G, An P, et al. APOL1 genetic variants in focal segmental glomerulosclerosis and HIV-associated nephropathy. J Am Soc Nephrol 2011;22:2129-37.  Back to cited text no. 17
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18.Seck SM, Gueye S, Diouf B. A new PKD-1 mutation discovered in a black African woman with autosomal polycystic kidney disease. Nephro-Urol Mon 2013;5:769-72 .  Back to cited text no. 18
    
19.Ahmed ER, Tashkandi MA, Nahrir S, Maulana A. Retrospective analysis of factors affecting the progression of chronic renal failure in adult polycystic kidney disease. Saudi J Kidney Dis Transpl 2006;17:511-5.  Back to cited text no. 19
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20.Davis ID, MacRae Dell K, Sweeney WE, Avner ED. Can progression of autosomal dominant or autosomal recessive polycystic kidney disease be prevented? Semin Nephrol 2001;21:430-40.  Back to cited text no. 20
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21.Grantham JJ, Mulamalla S, Swenson-Fields KI. Why kidneys fail in autosomal dominant polycystic kidney disease. Nat Rev Nephrol 2011;7:556-66.  Back to cited text no. 21
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22.Rahman E, Niaz FA, Al-Suwaida A, Nahrir S, Bashir M, Rahman H, et al. Analysis of causes of mortality in patients with autosomal dominant polycystic kidney disease: A single center study. Saudi J Kidney Dis Transpl 2009;20:806-10.  Back to cited text no. 22
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23.Chapman AB, Torres VE, Perrone RD, Steinman TI, Bae KT, Miller JP, et al. The HALT polycystic kidney disease trials: Design and implementation. Clin J Am Soc Nephrol 2010;5:102-9.  Back to cited text no. 23
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