Home About us Current issue Back issues Submission Instructions Advertise Contact Login   

Search Article 
  
Advanced search 
 
Saudi Journal of Kidney Diseases and Transplantation
Users online: 4097 Home Bookmark this page Print this page Email this page Small font sizeDefault font size Increase font size 
 

EDITORIAL Table of Contents   
Year : 1996  |  Volume : 7  |  Issue : 1  |  Page : 6-9
Tuberculosis in Hemodialysis Patients


Department of Nephrology and Dialysis, Al Hada Armed Forces Hospital, Taif, Saudi Arabia

Click here for correspondence address and email
 

How to cite this article:
Hussein M, Mooij J, Roujouleh H. Tuberculosis in Hemodialysis Patients. Saudi J Kidney Dis Transpl 1996;7:6-9

How to cite this URL:
Hussein M, Mooij J, Roujouleh H. Tuberculosis in Hemodialysis Patients. Saudi J Kidney Dis Transpl [serial online] 1996 [cited 2020 Sep 20];7:6-9. Available from: http://www.sjkdt.org/text.asp?1996/7/1/6/39531

   Introduction Top


There is a world-wide increase in the prevalence of tuberculosis (TB), due to several reasons including poverty, immi­gration, HIV-infection and the upsurge of drug-resistant strains [1],[2],[3],[4] . Patients with chronic renal failure are particularly at-risk for acquiring TB because of impaired cellular immunity [5] . This is especially important in areas where the disease is endemic. The presentation of TB in uremic patients might often be quite insidious and unusual, and diagnosis and management provides the treating physician with many special challenges.


   Epidemiology Top


In industrialized countries, the reported incidence of active TB in the general population is 10.4 per 100,000 per year [6] . Initial reports from these countries suggested no increase in the prevalence of TB among dialysis patients [7],[8] . However, an increased prevalence has been noted in subsequent reports [9],[10],[11],[12] . In Saudi Arabia, the incidence of active TB in the general population has been estimated to be around 30 per 100,000 per year [13] . A study of the World Health Organization (WHO) in 1984 found, among 4195 persons in the Gizan area, a prevalence of 2.2% of radiologically active disease. In the Riyadh area, among 1099 persons studied, the prevalence of TB was 2.3% in males and 1.9% in females [14] . Due to the high prevalence of TB in the general population in Saudi Arabia an increased prevalence would be expected in the dialysis population as well. Indeed, Al­Khader et al, reported in a survey of 50 dialysis centers in the Kingdom a pre­valence of active TB of 4.1% and in one center it was as high as 25% [15] . In our dialysis center, 32 out of 343 patients developed over a fourteen years period active TB giving a prevalence of 9.3%. A study from Jordan published in this issue of the journal [16] reports a prevalence of 1.2% among 927 patients on maintenance dialysis.

Majority of the patients reported in the literature developed symptoms of TB after being on dialysis for some time. This is in line with experimental findings which suggest that dialysis does not result in improvement in cellular immunity [5] . In our series, the duration of dialysis prior to development of symptoms was about one year [17] . Tuberculosis has been found to occur in patients with all kinds of renal diseases, and despite the well known association between diabetes mellitus and tuberculosis, especially pulmonary [18] , we found this association in only two of our 32 dialysis patients.

Tuberculosis is seen in all age-groups [17] , although the mean age of the patients with Tuberculosis in Hemodialysis Patients TB has been found to be slightly higher than that of the whole dialysis population. The distribution over the genders is approximately equal [15] .


   Diagnosis and Features Top


The diagnosis of TB is based on the finding of an acid fast bacilli positive smear, positive culture of Mycobacterium tuberculosis, typical histopathological findings and/or clinical presentation with positive response to anti-tuberculosis therapy [17] . Thus, all efforts should be made to obtain appropriate materials for culture, which should include sensitivity testing [2] . New techniques like the polymerase chain reaction (PCR) are promising diagnostic tools for the future [19] .

[Table - 1] shows the presenting features in our patients with TB. The onset is often insidious with anorexia, loss of weight and fever being the main symptoms [17] . In addition, the localization is frequently extra-pulmonary (in our study patients, 22/32 - 69%). Similar data have been reported by others including the group from Jordan [15],[16],[20] .

Tuberculous lymphadenitis was the predo­minant extra-pulmonary localization in our patients (12 of 32 patients), followed by peritoneal involvement (4 of 32), with single cases of spine, liver, genito-urinary and bone-marrow localization. Occult TB, defined as strong suspicion of the disease with negative routine and invasive investi­gations, failure to respond to broad-spectrum antibiotics and good response to anti­tuberculous therapy, was diagnosed in two patients. Pulmonary TB was found in 10 (31%) of our patients and was accompanied by pleural effusion in eight of them [17] .

The diagnosis of TB might be hampered by a negative purified protein derivative (PPD) skin test which according to some reports was the finding in a large number of patients [11],[12],[21],[22] . In our patients, a positive PPD skin test was seen in 62.5% of the cases [17] . We opine that in most of the cases, the result of PPD does not contribute much to the diagnosis or management. Also, no changes were found in hemoglobin and total or differential white blood cell count [17] . Thus, due to the frequent extra­pulmonary presentation, a high index of suspicion for TB is required coupled with a need for invasive procedures which in our patient-group included liver, bone, lymph node and peritoneal biopsies [17] .


   Treatment Top


One of the most widely used regimens for the treatment of TB is triple therapy with rifampicin (RMP), isoniazid (INH) and ethambutol (ETM) [20] . During the initial 10 years, we treated our patients with RMP and INH for 12 months, and ETM for three months in addition to pyridoxine at a dose of 40 mg per day [17] . However, during the last three years, in view of reports of increasing drug resistance, especially in the Western and Southern regions of Saudi Arabia [23] , we have begun to add pyrazinamide (PZA) to this regimen to be given for the initial three months only.

After the introduction of PZA, a reduction in the duration of treatment of pulmonary TB in the general population has become possible. Thus, INH, RMP, PZA and streptomycin or ETM are given for two months, and RMP and INH are continued thereafter for a total of six months [4],[24] . However, it is not clear whether this pro­tocol holds true for extra-pulmonary locali­zations and in uremic patients. We, there­fore, continue to treat our patients with RMP and INH for 12 months with ETM and PZA added for the first three months.

The dosage of RMP need not be altered in hemodialysis patients [20] . The half-life of INH in patients with renal failure varies from minimally elevated in fast acetylators, therefore requiring no dose modification, to significantly prolonged in slow acetylators [20] . Side-effects of INH include central and peripheral neurotoxicity [20],[25] . As the acetylator status is an investigation that is not readily available, we presume that all our patients are slow acetylators and give 70% of the standard dose of 5 mg/kg body weight (BW) per day. In view of dialyzer clearance, the drug is given after the dialysis session on dialysis days [17] . How­ever, recent reports suggest that INH is well tolerated even in slow acetylators with severe renal impairment and as such, no dose reduction is necessary [20] . Pyrazina­mide is given three times a week in a dosage of 40 mg/kg BW 24 hrs prior to a dialysis session [20] .

We give ETM in a dose of 15 mg/kg BW three times per week after each dialysis. Due to its toxic effects on the optic nerve, the visual acuity and color vision should be monitored prior to and regularly during treatment. Streptomycin is given in a dose of 750 mg three times per week 6-8 hours prior to dialysis [20] . In cases of multi-drug resistance, second-line medications like cycloserine, capreomycine, ethionamide and loxazine are available [26] . They all have their special toxicity and dose reduction is needed in severe renal insufficiency [27] .


   Prognosis Top


Previous reports on TB in dialysis patients indicated a high mortality of 11-75% caused mainly by miliary presentation and /or delay in initiation of therapy, due to a low index of suspicion with several patients diagnosed post-mortem [9],[10],[11],[12],[21] . In contrast, in our patient-group only one patient, non­compliant with the medication, developed disseminated tuberculosis (chest, peritoneum, central nervous system, urinary tract) and died. Patients were followed-up for up to 13 years and no recurrence was noted. Five patients of this group were transplanted and no recurrence was encountered during a follow-up of 3-7 years. Similar good results were seen in a survey of 64 patients in 50 dialysis centers in Saudi Arabia wherein complete resolution of the lesions occurred in 95.3% of the cases and there was only one death [15] .


   Conclusion Top


The lesson to be learnt from these observations is that there is an increased prevalence of TB among dialysis patients. However, with early diagnosis and treatment, the prognosis is good. Delayed diagnosis is invariably associated with a poor prognosis. Renal physicians should therefore, be aware of the unusual presentation and localization, and include TB in the differential diagnosis of a dialysis patient having non-specific symptoms like fever, anorexia, and weight loss. All efforts should then be made, including invasive investigations, to reach an early diagnosis.

 
   References Top

1.Dunlap N, Bailey WC. A catastrophe is brewing feditorian. Chest 1993:103:332-4.  Back to cited text no. 1    
2.Vas SI. Renaissance of tuberculosis in the 1990s: lessons for the nephrologist. Perit Dial Int 1994;14:209-14.  Back to cited text no. 2    
3.Bhatti N, Law MR, Morris JK, Halliday R, Moore-Gillon J. Increasing incidence of tuberculosis in England and Wales: a study of the likely causes. Br Med J 1995;310:967-9.  Back to cited text no. 3    
4.Lancet conference. The challenge of tuberculosis: statements of global control and prevention. Lancet 1995;346:809-19.  Back to cited text no. 4    
5.Descamps-Latscha B. Infection and immunity in end-stage renal disease. In: Henrich WL (ed). Principles and Practice of Dialysis. Baltimore, USA. Williams and Wilkins 1994;209-24.  Back to cited text no. 5    
6.Daneil THM. Tuberculosis. In: Isselbacher KJ, Braunwald E, Wilson JD, Martin JB, Fauci AS, Kasper DL (eds). Harrison's Principles of Internal Medicine, 13th Edition. New York, USA. McGraw-Hill Inc 1994;710-18.  Back to cited text no. 6    
7.Freeman RM, Newhouse CE, Lawton RL. Absence of tuberculosis in dialysis patients. JAMA 1975;233(13):1356.  Back to cited text no. 7    
8.Keane WF, Raij L. Infectious complications in maintenance dialysis patients. In: Drukker, Parsons, Maher (eds). Replacement of renal function by dialysis. The Hague, the Netherlands. Nijhoff 1978:621.  Back to cited text no. 8    
9.Pradhan RP, Katz LA, Nidus BD, Matalon R, Eisinger RP. Tuberculosis in dialyzed patients. JAMA 1974;229(7):798-800.  Back to cited text no. 9    
10.Sasaki S, Akiba T, Suenaga M, et al. Ten years' survey of dialysis-associated tuberculosis. Nephron 1979;24:141-5.  Back to cited text no. 10    
11.Lundin AP, Adler AJ, Berlyne GM, Friedman EA. Tuberculosis in patients undergoing maintenance hemodialysis. Am J Med 1979;67:597-602.  Back to cited text no. 11    
12.Andrew OT, Schoenfeld PY, Hopewell PC, Humphreys MH. Tuberculosis in patients with end-stage renal disease. Am J Med 1980;68:59-65.  Back to cited text no. 12    
13.Al-Kassimi FA. Review of tuberculosis in Saudi Arabia. Saudi Med J 1994;15(3):192-5.  Back to cited text no. 13    
14.Aneja KS. Assignment report tuberculosis in Saudi Arabia; March-May 1984. World Health Organisation- WHO-EM/TB/164 SAA/ESD/001:1984.  Back to cited text no. 14    
15.Al-Khader AA. Aswad S, Al-Sulaiman M, Babiksr MAR. Prevalence of tuberculosis in the dialysis population of Saudi Arabia. Saudi Kidney Dis Transplant Bull 1990;l(3):155-7.  Back to cited text no. 15    
16.Akash N, Smadi I, Hadidi M, Afara H, El ­Lozi M. Tuberculosis in patients on maintenance hemodialysis: a single center experience. Saudi J Kidney Dis Transplant 1996;7(l):20-23.  Back to cited text no. 16    
17.Hussein MM, Bakir N, Roujouleh H. Tuberculosis in patients undergoing maintenance dialysis. Ne-phrol Dial Transplant 1990;5:584-7.  Back to cited text no. 17    
18.Pandya L, Al-Sharif N, Maraey A, Al ­Majed S, El-Sakka M. Pulmonary tuberculosis in diabetic patients. Ann Saudi Med 1991;ll(3):293-6.  Back to cited text no. 18    
19.Barnes PF, Barrows SA. Tuberculosis in the 1990s. Ann Intern Med 1993;119:400­-10.  Back to cited text no. 19    
20.Ellard GA. Chemotherapy of tuberculosis for patients with renal impairment (editorial). Nephron 1993;64(2):169-81.  Back to cited text no. 20    
21.Papadimitriou M, Memmos D, Metaxas P. Tuberculosis in patients on regular hemodialysis. Nephron 1979;24:53-7.  Back to cited text no. 21    
22.Rutsky EA, Rostand SG. Mycobacteriosis in patients with chronic renal failure. Arch Intern Med 1980;140:57-61.  Back to cited text no. 22    
23.Jarallah JS, Elias AK. Al-Hajjaj MS, Bukhari MS, Al-Shareef AH, Al­ Shammari SA. High rate of rifampicin resistance of mycobacterium tuberculosis in the Taif region of Saudi Arabia. Tuber Lung Dis 1992;73:113-5.  Back to cited text no. 23    
24.Brausch LM, Bass JB Jr. The treatment of tuberculosis. Med Clin North Am 1993;77(6):1277-88.  Back to cited text no. 24    
25.Sulimani FA, Al-Daif AK, Mitwalli A, Huraib S. Isoniazid induced acute confusional state in a patient on hemodialysis. Saudi Kidney Dis Trans­plant Bull 1991;2(l):29-32.  Back to cited text no. 25    
26.Telzak EE, Sepkowitz KA, Alpert P, et al. Multi drug-resistant tuberculosis in patients without HIV infection. N Engl J Med 1995;333(14):907-ll.  Back to cited text no. 26    
27.Reese RE, Betts RF. Miscellaneous agents. In: Handbook of antibiotics. Boston, USA. Little Brown and company 1993;533-99.  Back to cited text no. 27    

Top
Correspondence Address:
Magdi Hussein
Department of Nephrology and Dialysis, Al Hada Armed Forces Hospital, P.O. Box 1347, Taif
Saudi Arabia
Login to access the Email id


PMID: 18417908

Rights and Permissions



 
 
    Tables

  [Table - 1]



 

Top
 
 
    Similar in PUBMED
    Search Pubmed for
    Search in Google Scholar for
    Email Alert *
    Add to My List *
* Registration required (free)  
 


 
    Introduction
    Epidemiology
    Diagnosis and Fe...
    Treatment
    Prognosis
    Conclusion
    References
    Article Tables
 

 Article Access Statistics
    Viewed2170    
    Printed53    
    Emailed0    
    PDF Downloaded263    
    Comments [Add]    

Recommend this journal