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Year : 2020  |  Volume : 22  |  Issue : 2  |  Page : 127-132

Obstructive uropathy and intrinsic renal disease in patients with benign prostatic obstruction: analysis of burden and associations in a university teaching hospital in Nigeria

Department of Surgery, Ahmadu Bello University/Ahmadu Bello University Teaching Hospital, Zaria, Kaduna State, Nigeria

Date of Submission24-Mar-2020
Date of Decision08-Apr-2020
Date of Acceptance07-May-2020
Date of Web Publication11-Sep-2020

Correspondence Address:
Dr. Musliu Adetola Tolani
Department of Surgery, Ahmadu Bello University/Ahmadu Bello University Teaching Hospital, Zaria, Kaduna State
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jomt.jomt_9_20

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Background: Benign Prostatic Hyperplasia (BPH) is a disease of the elderly. Some of the patients with this pathology could develop renal impairment due to the direct effect of obstruction or as a result of intrinsic renal disease. This study aimed to determine the burden and associations of obstructive uropathy and intrinsic renal disease in patients with benign prostatic obstruction in a university teaching hospital in Nigeria. Methods: This was a retrospective study of patients with BPH in our center. Glomerular Filtration Rate (GFR) was calculated and the severity of renal disease computed. Patients were classified as normal or those with obstructive uropathy and intrinsic renal disease. Patients’ age, diabetes mellitus presence and treatment given were also documented. Results: Obstructive uropathy and intrinsic renal disease occurred in 14 (15.1%) and 12 (12.9%) of the patients respectively. Nephropathy in the setting of obstruction occurred in four (4.3%) of the patients while the GFR was at stage 2 in obstructive uropathy patients who did not have renal impairment. Eight (10.4%) of the patients without nephropathy had diabetes mellitus. There was a significant inverse relationship between the age of presentation and the GFR (P = 0.001, odds ratio = −1.129). Initial urinary drainage delayed definitive surgery in all patients with obstructive nephropathy. Conclusion: The burden of nephropathy in BPH patients is quite considerable. A proportion of those without renal impairment harbour diabetes mellitus which could rapidly tilt obstructive uropathy patients into renal failure.

Keywords: Benign prostatic hyperplasia, glomerular filtration rate, nephropathy, obstruction

How to cite this article:
Tolani MA, Ahmed M, Nasir O, Sudi A. Obstructive uropathy and intrinsic renal disease in patients with benign prostatic obstruction: analysis of burden and associations in a university teaching hospital in Nigeria. J Med Trop 2020;22:127-32

How to cite this URL:
Tolani MA, Ahmed M, Nasir O, Sudi A. Obstructive uropathy and intrinsic renal disease in patients with benign prostatic obstruction: analysis of burden and associations in a university teaching hospital in Nigeria. J Med Trop [serial online] 2020 [cited 2022 Aug 18];22:127-32. Available from:

  Introduction Top

Benign Prostatic Hyperplasia (BPH) is a common urologic disease in the elderly.[1] Ojewola et al.[2] noted that its prevalence increased progressively from 104.3 per 1000 men in the fifth decade to 428.6 per 1000 men in the ninth decade of life. The burden of renal impairment is also high in older age groups.[3]

Nephropathy in the setting of BPH could be obstructive or non-obstructive. In the obstructive type, bladder outlet obstruction resulting from prostate enlargement triggers compensatory detrusor hypertrophy with inter-bundle collagen infiltrates which leads to either functional obstruction via persistent vesicoureteric reflux from decreased bladder compliance or mechanical obstruction from the development of intramural distal ureteric kinking.[4] The sequelae of this obstructive uropathy with progressive hydroureteronephrosis is a rise in the renal pelvis pressure causing renal cortical thinning with associated loss of nephrons and ultimately impaired renal function.[4] In the non-obstructive type, multiple co-morbidities including diabetes mellitus could cause intrinsic renal damage.[5]

Although renal impairment is a known complication of BPH, previous studies did not pay much attention to evaluating the burden of the types of nephropathy associated with it nor did they document the severity of renal damage in these patients. Furthermore, the characterization of the degree of renal dysfunction in patients with obstructive uropathy who have not developed renal insufficiency is lacking in these studies. The aim of this study was to evaluate the burden and associations of obstructive uropathy and intrinsic renal disease in patients with benign prostatic obstruction in a university teaching hospital in Nigeria.

  Material and methods Top

This was a retrospective study carried out in Ahmadu Bello University Teaching Hospital, Zaria, a tertiary hospital with a total bed capacity of 700 located in Kaduna State, Nigeria. It provides clinical services to people of this state and other neighbouring states. Ethical approval was obtained from our Institutional Health Research Ethics Committee. All patients who were 40 years and above and presented with Lower Urinary Tract Symptoms (LUTS) due to BPH between January 2016 and January 2019 were included. Those with co-existing urethral stricture, neurogenic bladder, bladder cancer or histological diagnosis of prostate cancer were excluded.

Information on patient’s age, diabetes mellitus, presence of hematuria and treatment offered were extracted from the medical record. Evidence of Urinary Tract Infection (UTI) was obtained from microbiologic culture of the infective organism and documented. Results of Packed Cell Volume, PCV (%), serum urea (mmol/l) and serum creatinine (μmol/l) were documented. The presence of hydronephrosis, as seen on abdominal ultrasound scanning with a 3.5 Hz end-firing probe, was also recorded.

The estimated Glomerular Filtration Rate (GFR) was calculated from serum creatinine, Scr (μmol/l), using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) formula for adult black males (for Scr≤79.6 μmol/l: GFR = 141 × min(Scr/79.6)−0.411 × 0.993Age × 1.159 [if black] and Scr>79.6 μmol/l: GFR = 141 × max(Scr/79.6)−1.209 × 0.993Age × 1.159 [if black]) and was expressed in ml/min/1.73m2.[6]

Anemia was defined as PCV less than 30%. Renal impairment was defined as estimated GFR <60ml/min/1.73m2 while patients with estimated GFR ≥60 ml/min/1.73m2 were considered as those without nephropathy.[7] Obstructive uropathy was defined by the ultrasound confirmation of unilateral or bilateral hydronephrosis in patients with benign prostatic obstruction. It was further divided into obstructive nephropathy, when hydronephrosis was associated with the presence of renal impairment, and, obstructive uropathy only, when hydronephrosis was not associated with renal impairment.[8] Intrinsic renal disease or non-obstructive nephropathy was defined as the absence of hydronephrosis in those with renal impairment. Normal patients were recognized based on the absence of both hydronephrosis and renal impairment. GFR was classified based on the Kidney Disease: Improving Global Outcomes (KDIGO) 2012 GFR categories as follows: stage 1 (GFR of ≥90 ml/min/1.73m2), stage 2 (GFR of 60–89 ml/min/1.73m2), stage 3 (GFR of 30–59 ml/min/1.73m2), stage 4 (GFR of 15–29 ml/min/1.73m2) and stage 5 (GFR <15 ml/min/1.73m2).[7]

Data were analyzed using Statistical Package for the Social Sciences (SPSS) software, version 20.0 (IBM Corp., Armonk, New York, USA). It was summarized by the status of renal function using mean and standard deviation (parametric data) and median and interquartile range (non-parametric data) for continuous variables and frequencies with percentages for categorical variables. Comparisons were made using independent samples t-test and Mann-Whitney U test for continuous variables, and Chi-square test and Fischer’s exact test for categorical variables as appropriate. Correlation between the estimated GFR and the age of presentation was done using Pearson’s correlation test and linear regression analysis was done to further test this association. Kruskal-Wallis test was used to compare the estimated GFR across prostate volume groups classified in tertiles. The P-value was considered to be significant if < 0.05.

  Results Top

The data of 120 patients were obtained. Twenty-seven patients were excluded as a result of incomplete records and 93 patients were finally analyzed.

Sixteen (17.2%) of BPH patients had renal impairment giving an estimated prevalence rate of 172 per 1000 men. Obstructive uropathy occurred in 14 (15.1%) of the patients while 12 (12.9%) of them had intrinsic renal disease. Nephropathy in the setting of obstruction occurred in 4 (4.3%) of the patients. In patients without renal impairment, the estimated GFR was significantly lower in the obstructive uropathy group (72.5 ml/min/1.73m2 versus 97.8 ml/min/1.73m2, P = 0.024). The highest rate of diabetes mellitus occurred in those with intrinsic renal disease, 3 (25.0%) while in obstructive uropathy and normal patients, 1 (10.0%) and 7 (10.4%) of them had diabetes mellitus respectively [Table 1].
Table 1: Characteristics of the BPH patients according to their renal status (N = 93)

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The stages of GFR in patients with obstructive uropathy (without renal impairment), obstructive nephropathy and intrinsic renal disease are shown in [Figure 1]. There was a significant relationship between the GFR stages and these conditions in patients with BPH (P = 0.001). The correlation between the age at presentation and the estimated GFR of the patients is displayed in [Figure 2]. A significant association was observed between the age of presentation and the estimated GFR on regression analysis (P = 0.001, Odds Ratio = −1.129, 95% Confidence Interval = −1.801 to −0.457). Although there was decreased renal function at large prostate volumes, this relationship was not significant (P = 0.652) [Figure 3].
Figure 1: Stages of Glomerular Filtration Rate in different group of patients with benign prostatic obstruction (N = 93).

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Figure 2: Correlation between the age at presentation and the estimated GFR of the patients.

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Figure 3: Mean estimated Glomerular Filtration Rate of the patients at different prostate volumes.

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The PCV was significantly lower in those with obstructive nephropathy compared to those with intrinsic renal disease (28.8% versus 36.5%, P = 0.039). The mean PCV was however higher (39%) in patients without nephropathy. Other complications of BPH according to the renal status are displayed in [Table 2].
Table 2: Occurrence of BPH complications according to renal status

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Temporary urine drainage was used in five (55.6%) of those with intrinsic renal disease and three (33.3%) of those with obstructive uropathy (who had no renal impairment) for the relief of LUTS. It was however carried out in all the patients with obstructive nephropathy before definitive treatment was offered to them. Renal recovery was however incomplete in one (25.0%) of the obstructive nephropathy patients following urinary drainage warranting hemodialysis as renal replacement therapy. With regards to definitive therapy in nephropathy patients and compared to those without renal damage, a larger proportion of those with renal impairment had surgical treatment of BPH (28.6% versus 23.2%).

  Discussion Top

This study revealed that about one in five patients (17.2%) with BPH had renal impairment which is in consonance with the work of Rule et al.[1] where 21% of those with BPH had chronic kidney disease. Although Ogbonna et al.[9] and Hong et al.[10] reported different rates of 29.5% and 5.9% respectively, this might be related to the use of and variation in the cut-off value of serum creatinine that defined renal dysfunction in their studies. GFR is a better measure of renal status compared to serum creatinine due to tubular secretion in the latter measure.[4]

Majority of the nephropathy in this present study was of non-obstructive pathology, which supports the assertion of Madersbacher et al.[5] that comorbidities like diabetes mellitus is the most likely cause of renal compromise in the setting of Bladder Outlet Obstruction. This does not undermine the importance of the finding of 4.3% hospital prevalence rate of obstructive nephropathy in this work which is close to the range of 4.4% to 11.0% documented in adults.[8] It probably highlights the sequelae of late patient presentation in this domain because more than double of this proportion (10.8%) had obstructive uropathy with Stage 2 estimated GFR, thus, constituting another waiting pool for the development of renal damage. In addition, a larger proportion of patients with GFR <15 ml/min/1.73 m2 had obstructive nephropathy (50%) in comparison to just below one-tenth of this percentage (8%) who had intrinsic renal disease. Adejumo et al.[8] observed that 70% of their obstructive nephropathy patients had Stage 5 estimated GFR. The difference in these proportions might reflect variation in the profile of patients studied. While our patient population was BPH patients, 60% of their patients had advanced cancer. However, it reiterates the importance of setting early prevention measures to reduce obstructive nephropathy as instituted for other leading causes of renal failure.[8]

Decrease in renal function has long been associated with aging. The significant negative correlation between the estimated GFR and age of presentation noted in this study is similar to the finding of Lee et al.[3] in their study on patients with LUTS/BPH. This thus supports Ponholzer et al.’s[11] inference that age is a significant determinant of decreased GFR. On the other hand, an increase in the total prostate volume was not significantly related to a decrease in estimated GFR. Other researchers have made similar observations on this.[3],[12] It might be because the degree of obstruction, and not the prostate volume, is the primary determinant of the severity of renal impairment.[1],[4] Furthermore, the high proportion of diabetes mellitus (27.3%) in patients with intrinsic renal disease suggests its role as an etiological factor for the disease condition. Unlike this study, a previous investigation which showed significant difference in the report of diabetes mellitus between those with and those without renal impairment (17.4% versus 7.0%, P < 0.001) might be a result of the relatively larger sample size of patients in that study.[10]

The significantly greater severity of anemia in the obstructive nephropathy patients could be due to worse mean estimated GFR (in the severe range) in them. It is of note that renal impairment could lead to uremic toxin-induced bone marrow suppression and erythropoietin deficiency.[13] Also, UTI was quite high (50.0%) in the setting of obstructive nephropathy in comparison to the rates seen in other patients in this study. Urine stasis could be a promoting factor for bacterial colonization and subsequent infection.[8] This could then be the pathologic factor in the chronic interstitial nephritis observed in obstructive nephropathy patients.[14] The use of lower urinary tract drainage is necessary in obstructive nephropathy for the recovery of renal function.[9] It is therefore not surprising that 100% of these patients had initial urine drainage before definitive surgery. Renal recovery in these cases could however be incomplete as 25% of the obstructive nephropathy patients had hemodialysis as renal replacement therapy. Poor renal recovery on urine drainage may be related to the duration of LUTS, presence of associated UTI and thinning of the renal parenchyma.[15] Urethral catheterization or suprapubic cystostomy in other patients in this study probably arose from the need for the temporary relief of the significant bothersome LUTS that characterized this study population. Surgical treatment for BPH was employed more in those with nephropathy as a permanent measure for bladder outlet obstruction relief. This is important due to the risk of UTI from an indwelling catheter that could worsen renal function. Initial urine drainage and further renal replacement therapy could increase the cost of hospital stay and cause a delay in surgery as evident by nearly three-quarters of patients on surgery waiting list in comparison to those without renal damage who were already on medical therapy for BPH.[9]

This study has some limitations. It was a retrospective study with its associated challenges during data collection from paper records. Despite adjustments in the formulas for the calculation of estimated GFR, it might not be the most accurate measure of renal function. The degree of bladder outlet obstruction as indicated by pressure-flow urodynamic study, which is directly related to renal functional status, was not measured in this study.

The prevalence of nephropathy in BPH patients is 172 per 1000 men with the occurrence of intrinsic renal disease almost thrice that of obstructive nephropathy. Although temporary lower urinary tract drainage is necessary for renal recovery in obstructive nephropathy patients, it may delay their time for definitive surgery. There is a need for the institution of early management and other preventive measures in elderly men with obstructive uropathy in order to prevent their progression to renal impairment.

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  References Top

Rule AD, Jacobson DJ, Roberts RO, Girman CJ, McGree ME, Lieber MM et al. The association between benign prostatic hyperplasia and chronic kidney disease in community-dwelling men. Kidney Int 2005;67:2376-82.  Back to cited text no. 1
Ojewola RW, Oridota ES, Balogun OS, Alabi TO, Ajayi AI, Olajide TA et al. Prevalence of clinical benign prostatic hyperplasia amongst community-dwelling men in a South-Western Nigerian rural setting: a cross-sectional study. African J Urol 2017;23:109-15.  Back to cited text no. 2
Lee JH, Kwon H, Park YW, Cho IC, Min SK. Relationship of estimated glomerular filtration rate with lower urinary tract symptoms/benign prostatic hyperplasia measures in middle-aged men with moderate to severe lower urinary tract symptoms. Urology 2013;82:1381-5.  Back to cited text no. 3
Udoh E, Ekanem A. Pattern of serum creatinine and urea in patients seen with symptoms of bladder outlet obstruction. Saudi J Med Pharm Sci 2016;2:185-9.  Back to cited text no. 4
Madersbacher S, Alivizatos G, Nordling J, Sanz CR, Emberton M, de la Rosette J. EAU 2004 Guidelines on assessment, therapy and follow-up of men with lower urinary tract symptoms suggestive of Benign Prostatic Obstruction (BPH Guidelines). Eur Urol 2004;46:547-54.  Back to cited text no. 5
Levey AS, Stevens LA, Schmid CH, Zhang Y, Castro AF, Feldman HI et al. A new equation to estimate glomerular filtration rate. Ann Intern Med 2009;150:604-2.  Back to cited text no. 6
Kidney Disease: Improving Global Outcomes (KDIGO) CKD Work Group. KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease. Kidney Int Suppl 2013;3:1-150.  Back to cited text no. 7
Adejumo OA, Akinbodewa AA, Okaka EI, Alli OE, Abolarin OS. Obstructive nephropathy in a kidney care hospital in Southwest Nigeria: the need for early screening and prevention. J Med Trop 2017;19:98-103.  Back to cited text no. 8
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Ogbonna BC, Madziga AG, Anteyi EA. The impact of renal impairment on the management of patients with lower urinary tract obstruction. Trop Doct 1997;27:75-7.  Back to cited text no. 9
Hong SK, Lee ST, Jeong SJ, Byun S, Hong YK, Park DS et al. Chronic kidney disease among men with lower urinary tract symptoms due to benign prostatic hyperplasia. BJU Int 2009;105:1424-8.  Back to cited text no. 10
Ponholzer A, Temml C, Obermayr RP, Rauchenwald M, Madersbacher S. The association between lower urinary tract symptoms and renal function in men: a cross-sectional and 5-year longitudinal analysis. J Urol 2006;175:1398-402.  Back to cited text no. 11
Nazar M, Yunus KK, Sankar AK, Ram SHS, Radhakrishnan V, Madan A et al. Prostate gland volume and its relationship to complications of benign prostatic enlargement. IOSR J Dent Med Sci 2015;14:33-7.  Back to cited text no. 12
Mudiyammanavara RN, Dhananjaya PE, Agarwal R. Cross sectional study of anaemia in chronic kidney disease. Indian J Basic Appl Med Res 2015;4:414-9.  Back to cited text no. 13
Speakman MJ, Cheng X. Management of the complications of BPH/BOO. Indian J Urol 2014;30:208-13.  Back to cited text no. 14
[PUBMED]  [Full text]  
Rule AD, Lieber MM, Jacobsen SJ. Is benign prostatic hyperplasia a risk factor for chronic renal failure? J Urol 2005;173:691-6.  Back to cited text no. 15


  [Figure 1], [Figure 2], [Figure 3]

  [Table 1], [Table 2]


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