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Saudi Journal of Kidney Diseases and Transplantation
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RENAL DATA FROM THE ASIA - AFRICA Table of Contents   
Year : 2010  |  Volume : 21  |  Issue : 6  |  Page : 1172-1178
Prevalence and pattern of cystic kidney diseases in Ilorin, Nigeria


1 Department of Medicine, University of Ilorin Teaching Hospital, Ilorin, Nigeria
2 Department of Radiology, University of Ilorin Teaching Hospital, Ilorin, Nigeria

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Date of Web Publication4-Nov-2010
 

   Abstract 

Cystic kidney disease is an important cause of chronic renal failure. Since the utili­zation of imaging techniques in the diagnosis of diseases has become widespread, cystic kidney disease is now being increasingly diagnosed. This study is designed to determine the prevalence and pattern of cystic kidney disease at the Nephrology Unit of University of Ilorin Teaching Hospital (UITH), Ilorin. All consecutive adult patients seen in the Nephrology Unit of UITH during a ten-year period (January 1999-December 2008) were studied for the presence of cystic kidney disease. The results were analyzed with specific reference to age, gender, annual inci­dence, type of cystic disease, location of cyst, mode of presentation, complications and prognosis. A total of 67 out of 436 renal patients (15.4%) studied had cystic kidney disease. A progressive annual increase in the number of cases was noticed. The age-range was 20-83 years with a mean of 47.4 +/- 16.2 years and the peak incidence was in the third and sixth decades with male to female ratio of 1.3:1. The types of cystic kidney disease identified in the study were: 26 simple cysts (38.8%), 35 polycystic kidney disease (53.3%) and six multicystic kidney disease (8.9%). The most common mode of presentation was abdominal pain followed by hypertension, urinary tract infection, chronic renal failure and palpable abdominal mass, in decreasing order. Our study indicates that cystic kidney disease is not an uncommon problem among our renal patients and the incidence is on the increase. Although, routine screening of family members with cystic kidney disease still remains a contentious issue because the knowledge may evoke anxiety in terms of employment and insurance, screening of symptomatic cases or those that develop hypertension, hematuria and proteinuria is strongly recommended.

How to cite this article:
Chijioke A, Aderibigbe A, Olarenwaju TO, Makusidi AM, Oguntoyinbo AE. Prevalence and pattern of cystic kidney diseases in Ilorin, Nigeria. Saudi J Kidney Dis Transpl 2010;21:1172-8

How to cite this URL:
Chijioke A, Aderibigbe A, Olarenwaju TO, Makusidi AM, Oguntoyinbo AE. Prevalence and pattern of cystic kidney diseases in Ilorin, Nigeria. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2020 Oct 22];21:1172-8. Available from: https://www.sjkdt.org/text.asp?2010/21/6/1172/72320

   Introduction Top


There is very little information on the preva­lence and pattern of cystic kidney disease in Nigeria. Most of the available studies on cystic kidney disease seem to focus on polycystic kidney disease, especially of the autosomal do­minant type. This is probably because auto­somal dominant polycystic kidney disease (ADPKD) is one of the most common here­ditary disorders with extra-renal complications and an important cause of end-stage renal di­sease (ESRD) in Caucasians. [1],[2],[3],[4] Also, simple renal cysts, which are the most common in human kidneys, are largely asymptomatic, they are adjudged to be of little clinical signifi­cance. Although ADPKD is said to be rare in Blacks, [6],[7],[8] its incidence in Blacks and Cauca­sians in some studies is almost simi-lar. [10],[11] It is difficult to explain the racial differences in the prevalence of ADPKD as the disease is a hereditary disorder. It is possible that Cauca­sian polycystic kidney disease tends to run a more progressive course, either diagnosed early or that the extra-renal complications are better managed, thus allowing them to live long enough to develop ESRD. It is also possible that most Blacks die from extra-renal compli­cations before the onset of ESRD.

The paucity of data on cystic kidney disease in Nigeria tends to give credence to the assumption that it is rare among our renal pa­tients. Since ultrasound machines have become readily available in most health-care facilities in the last decade, renal ultrasonographic tech­niques have been utilized to evaluate all pa­tients seen in our nephrology unit irrespective of the clinical features at presentation, inclu­ding those that initially presented to other units or general practitioners with other conditions. The present study was performed to determine the prevalence, clinical pattern and renal prog­nosis of cystic kidney disease in Ilorin, Nigeria.


   Patients and Methods Top


All consecutive adult patients seen in the nephrology unit of the University of Ilorin Teaching Hospital (UITH), Ilorin over a 10­year period (January 1999-December 2008) were prospectively studied. The presence of cystic kidney disease was evaluated by de­tailed history, thorough physical examination, abdominal ultrasound and intravenous uro­graphy (IVU). Blood and urine samples were collected from all patients for full blood count, erythrocyte sedimentation rate (ESR), serum creatinine and blood urea, urine analysis, urine microscopy and culture and 24-hour urine col­lection for protein estimation and creatinine clearance.

The criteria for the diagnosis of polycystic kidney disease included most of the following: presence of at least three bilateral renal cysts, presence of cysts in other abdominal organs, positive family history of dominantly expressed renal cystic diseases, documentation of extra­renal manifestation of the disease, presence of the culprit gene by gene linkage analysis, in­travenous urographic demonstration of thin­ning and angulation of the collecting system and a moth-eaten appearance of the cortex, en­larged kidneys with multiple echofree areas in both kidneys and impaired urine concentrating ability.

Simple renal cyst was diagnosed with most of the following: absence of heredity, normal renal function, usually few unilateral or bila­teral spherical and unilocular cysts, non-com­munication with renal pelvis, thin and smooth walled transparent cysts and homogeneous atte­nuation without contrast enhancement on CT scan. Multicystic kidney disease was recog­nized by the presence of many cysts that are localized to one kidney without intervening normal renal tissues, loose binding of the cysts by primitive mesenchymal tissues, absence of excretory function by IVU, congenital abnor­mality of the contralateral kidney, rings of cal­cification in the cyst wall, no extra-renal cysts or family history of cystic kidney disease.

It was not possible to sonographically screen family members of those with polycystic kid­ney disease because of lack of co-operation and refusal by the first degree relatives to un­dergo screening. Routine screening of family members of patients with cystic renal disease still remains a contentious issue as the know­ledge may evoke anxiety, decreased job oppor­tunity and reduced insurance facility.


   Results Top


Sixty-seven out of 436 (15.4%) renal patients seen during the study period had cystic kidney disease. The data showed progressive yearly increase in the number of cases [Figure 1]. [Table 1] shows that the age-range was 20 to 83 years, with a mean of 47.4 ± 16.2 years. The peak age incidence was in the third and sixth decades with male to female ratio of 1.3:1. The types of cystic kidney disease seen included 26 simple renal cysts (38.8%), 35 polycystic kid­ney disease (53.3%) and six multicystic kidney diseases (8.9%) [Figure 2],[Figure 3],[Figure 4] and [Table 2]. Majority of the simple renal cysts (77%) and the six multicystic kidneys were unilateral and seen in the right kidney. The most common mode of presentation was abdominal pain fol­lowed by hypertension, urinary tract infection, chronic renal failure and abdominal mass, in decreasing order [Table 3]. Majority of the po­lycystic kidney disease patients presented with renal and extra-renal features of the disease and high rate of case fatality. The 10% morta­lity recorded in the study was due to polycystic kidney disease with the terminal event being chronic renal failure in majority of cases. This is because most of them presented late when the kidneys are already palpably enlarged with sustained high blood pressure and clinical or investigative features of renal insufficiency.
Table 1 :Age and sex distribution of the study patients.

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Table 2 :Type of renal cysts and their location in the study patients.

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Table 3 :Mode of presentation of renal cysts in the study patients.

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Figure 1 :Yearly incidence of cystic kidney disease in our study.

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Figure 2 :Sonographic picture of a simple renal cortical cyst.

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Figure 3 :Sonographic picture of polycystic kidney disease.

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Figure 4 :Sonographic picture of multicystic kidney.

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   Discussion Top


Cystic kidney disease is a common cause of morbidity and mortality worldwide. The pre­valence rate of 15.4% observed in this study shows that it is not uncommon and is com­parable with rates reported from other parts of the world. [4],[5] However, after the first two years, we noted a progressive annual increase in the number of patients with cystic kidney disease. This may be a reflection of increased utili­zation of imaging techniques in the investiga­tion of abdominal symptoms and in patients presenting with renal diseases of diverse etio­logies. The most frequently used methods for diagnosis are ultrasonography, computerized tomography and magnetic resonance imaging but the high sensitivity of ultrasonography and the fact that it neither uses radiation nor con­trast material and its low cost makes it the preferred diagnostic method in most studies. The major flaw of imaging techniques is that they will not identify gene carriers in those suspected to have hereditary renal cystic di­sease whose renal cysts have not yet become large enough to be detected. About 11-24% of gene carriers of ADPKD do not have ultra­sound detectable renal cysts before the age of 30 years but CT scan with contrast enhance­ment may diagnose some cases missed by ultrasonography. [12],[13] However, in persons at risk of cystic kidney disease, who have no sonographically defined cyst, gene linkage tech­niques can be useful. [14] Also, perinatal diag­nosis is possible with the use of DNA obtained by amniocentesis or chorionic-villus sampling. [15] As a result of expense of gene linkage tech­niques, the need to involve other members and the reliability of ultrasonography, gene linkage will probably be limited to situations in which family planning would be altered or for po­tential kidney donors in whom ultrasound fin­dings are non-diagnostic. [16],[17]

The mean age of 47.4 ± 16.2 years and male to female ratio of 1.3:1 noted in this study is in keeping with findings by some other authors. [4],[5],[10],[11] The prevalence of cystic kidney disease increases with age, occurring more frequently in adults over 56 years of age, [5],[18],[19] and shows equal gender distribution although males appear to manifest more severe disease. [4],[5] Simple re­nal cysts and polycystic kidney disease cons­tituted 38.8% and 53.3% respectively while multicystic kidney disease accounted for 8.9% in this study. This may have to do with the group of patients studied as they were mainly renal patients in a hospital setting in contrast with general population studies in which simple cysts were found to be more common than polycystic kidney disease. [5],[20]

Simple cysts are the commonest of all renal cysts with unknown cause. They are likely acquired rather than congenital because they are rarely found in children but become in­creasingly common with advancing age. They are largely asymptomatic but may present with abdominal pain, abdominal mass, hematuria, hypertension and erythrocytosis while some are complicated by infection, hemorrhage and renal insufficiency. [20],[21],[22],[23],[24],[25] Majority of simple re­nal cysts in this study presented with abdomi­nal pain (78%) followed by hypertension (36%) urinary tract infection (28%) and as incidental finding in 21%. Many of the cases with abdo­minal pain may not have been related to simple renal cysts as patients with abdominal pain of diverse causes are often subjected to ultrasonography of the abdomen. The associa­ted hypertension in simple renal cyst is thought to be due to activation of renin-angiotensin system from disruption of the renal vasculature by cysts with subsequent development of intra­renal ischemia. Hematuria and abdominal mass as presenting features were not observed in this study.

Polycystic kidney disease, especially the autosomal dominant type is a systemic disease with both renal and extra-renal manifestations. The common clinical renal features are: chronic loin pains, hematuria, infection, nephrolithiasis and hypertension while the most common extra-renal manifestation is hepatic cysts. [26],[27]

Although, our patients with polycystic kidney disease were not subjected to gene linkage analysis, most met the clinical criteria for the diagnosis of ADPKD. [12] Abdominal pain, he­maturia and hypertension were observed to occur more often in patients with large kid­neys. The commonest mode of presentation in our polycystic kidney patients was abdominal pain (70%) followed by hypertension (47%), urinary tract infection (33%), chronic renal fai­lure (13%), abdominal mass (10%), incidental findings (10%) and hematuria (3%). The mode of presentation of ADPKD tends to vary in different studies. Rale et al noted that heavi­ness and pain in the flanks which is often associated with hematuria and urinary tract infection were the main features while Lopez­Alvarez et al [29] and Martinez Maldonado et al, [30] observed that the hallmark of the disease was impaired concentrating ability manifesting as urinary frequency and nocturia. In another re­lated study by Dalgaard et al, [31] hematuria was found to be the most common mode of pre­sentation followed by hypertension and palpa­ble renal mass. However, in many cases, diag­nosis is only made post mortem although pa­tient may have suffered from one of the com­plications for years. However, complications like hypertension and chronic renal failure may develop from three to twelve years after the diagnosis of ADPKD has been made. [32] It is also pertinent to note that family history may be absent in some cases of proven ADPKD. [33]

Mortality rate of 10% recorded in this study were in polycystic kidney disease patients and the terminal event was ESRD. Polycystic kid­ney disease is a common cause of ESRD and studies have shown that by the age of 60 years, more than 50% will have reached ESRD. [34],[35]

There were six cases of multicystic kidney disease seen in this study and all of them pre­sented with only abdominal pain. Multicystic kidney disease denotes a severe form of renal dysplasia which is invariably associated with partial atresia or even absence of the ureter. [36],[37]

The cysts are loosely bound by primitive me­senchymal tissue which contains some meta­nephric elements. It is completely functionless and bears no resemblance to normal renal tissue. Bilateral forms are incompatible with life while unilateral disease may be an inciden­tal finding in adults although some may pre­sent with asymptomatic abdominal mass. One of our cases had hydronephrosis of the contra­lateral side while others had hydroureters.

We conclude that cystic kidney disease is an important and common cause of morbidity and mortality world wide and the incidence is on the increase in our environment. Although rou­tine screening of family members of patients with cystic kidney disease still remains a con­tentious issue, we strongly recommend that symptomatic family members or those that de­velop hypertension, hematuria and/or proteinu­ria should be screened.

 
   References Top

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2.Fick GM, Johnson AM, Hammond WS, Gabow PA. Causes of death in autosomal dominant polycystic kidney disease. J Am Soc Nephrol 1995;5:2038-56.  Back to cited text no. 2
    
3.Torra R, Darnell A, Cleries M, et al. Polycystic Kidney Disease patients on renal replacement therapy. Data from Catalan Renal Registry. Contrib Nephrol 1995;115:127-81.  Back to cited text no. 3
    
4.Carcia IC, Torres VE, Offord KP, et al. Epide­miology of adult polycystic kidney disease. Olmsted country Minesote. 1935-1980. Am J Kidney Dis 1983;2:630-9.  Back to cited text no. 4
    
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11.The demographics of ESRD in USRDS 1990 annual data report. Bethesda Md. National Ins­titute of Health. National Institute of Diabetics and Digestive and kidney Diseases. 1990;17-­22.  Back to cited text no. 11
    
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15.Readers ST, Zerres K, Gal A, et al. Prenatal diagnosis of autosomal dominant polycystic kidney disease with a DNA probe. Lancet 1986;2:6-8.  Back to cited text no. 15
    
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17.Hanning VL, Hopkins JR, Johnson HK, Philips JA, Readers ST. Presymptomatic testing of adult onset polycystic kidney disease in at risk kidney transplant donors. Am J Med Genet 1991;40:425-8.  Back to cited text no. 17
    
18.Bear JC, McManamon P, Morgan J, et al. Age at clinical onset and its ultrasonographic detec­tion of adult polycystic kidney disease. Data for genetic counseling. Am J Med Genet 1984; 18:45-53.  Back to cited text no. 18
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21.Jafar A, Michael AB, Moghazi S, et al. Re­duced renal function in patients with simple renal cysts. Kidney Int 2004;65(6):1523-755.  Back to cited text no. 21
    
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26.Gabour PA. Autosomal dominant polycystic kidney disease more than a renal disease. Am J Kidney Dis 1990;16:403-13.  Back to cited text no. 26
    
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28.Rale JE, Odell HM, Congenital polycystic di­sease of the kidney: Review of Interactive and data on 207 cases. Am J Med Sci 1949;218: 399-406.  Back to cited text no. 28
    
29.Lopez-Alzrez R. The complications that develop from polycystic kidney disease of the kidneys: 154 personal observations. Press Med 1964;72: 1583-5.  Back to cited text no. 29
    
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31.Dalgaard OZ. Bilateral polycystic kidney disease: A follow up of 284 patients and their families. Acta Med Scand 1957;3280(Suppl): 1-28.  Back to cited text no. 31
    
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35.Gabow PA, Johnson AM, Kasha WD, et al. Factors effecting the progression of renal disease in ADPKD. Kidney Int 1992;41:1311-­9.  Back to cited text no. 35
    
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Correspondence Address:
Adindu Chijioke
Department of Medicine, Baboko Post Office, P.O. Box 13945, Ilorin
Nigeria
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    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4]
 
 
    Tables

  [Table 1], [Table 2], [Table 3]

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