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Saudi Journal of Kidney Diseases and Transplantation
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Year : 1998  |  Volume : 9  |  Issue : 3  |  Page : 301-305
Acute Renal Failure in Jordan


Department of Medicine, Jordan Hospital, Amman, Jordan

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   Abstract 

We evaluated 215 patients with acute renal failure (ARF) in three centers in Jordan over an 18 months period. Their ages ranged between 12-90 years, and 120 of them were males. Parenchymal renal insult was the commonest cause of ARF as it was seen in 125 patients (58%). Pre-renal azotemia was seen in 60 patients (28%) and acute obstructive uropathy in 30 patients (14%). At presentation, 152 patients (70.7%) were oligo-anuric, while 63 (29.3%) were non-oliguric. Forty patients (18.6%) required dialysis support; 30 of them were in the renal failure group (75%). Thirty-two of the 40 patients were oliguric­aruric. Complete recovery of renal function was achieved in 80% for the whole group, and in 64% of those with parenchymal renal insult. Forty-seven patients (21.9%) died; 35 of them (63.9%) were in the renal group, and 37 patients (78%) were oligo-anuric. Sepsis and cardiac complications were together responsible for almost 75% of the deaths.

Keywords: Renal failure, Acute, Jordan.

How to cite this article:
Said R. Acute Renal Failure in Jordan. Saudi J Kidney Dis Transpl 1998;9:301-5

How to cite this URL:
Said R. Acute Renal Failure in Jordan. Saudi J Kidney Dis Transpl [serial online] 1998 [cited 2019 Nov 22];9:301-5. Available from: http://www.sjkdt.org/text.asp?1998/9/3/301/39275

   Introduction Top


Acute renal failure (ARF) is a medical emergency defined as an abrupt decline in kidney function resulting in retention of nitrogenous wastes, irrespective of urine volume. It is easily recognized by rapidly rising serum creatinine and blood urea nitrogen [1],[2],[3] . It is usually reversible by early diagnosis and correct management, but still carries a high mortality rate despite the excellent progress in the methods of renal replacement therapy [4],[5],[6],[7] . ARF may be associated with anuria (urine volume less than 100 cc per 24 hours), oliguria (urine volume <500 cc/24 hours) or non-oliguria (urine volume >500 cc/24 hours) [7],[8] . It is customary to classify ARF into three major groups, pre-renal, renal and post-renal [10],[11] .

In this report, we evaluate acute renal failure in Jordan, with special reference to the etiological factors and outcome.


   Materials and Methods Top


A total of 215 patients, with no previous history of renal failure, were evaluated for developing ARF at three different hospitals in Amman, Jordan during the period from September 1996-through March 1998.

Sixty-three patients were seen at Jordan University Hospital, 72 at the Islamic Hospital and 80 at Jordan Hospital; the last two are private hospitals. There were 120 male and 95 females, and their ages ranged between 12 and 90 years.

All patients had complete history and physical examinations, and particular attention was paid to drugs that may predispose to ARF. Laboratory investigations included urinalysis, serum electrolytes, urine electrolytes, ultra­sound of kidneys and bladder and kidney biopsy as indicated. In addition, manage­ment including dialysis and outcome were evaluated.


   Results Top


There were 145 patients who acquired ARF during the course of their hospital admission for other reasons, while the other 70 patients were admitted primarily with ARF. Sixty patients (28%) had pre-renal azotemia, 30 patients (14%) had post-renal ARF and 125 patients (58%) renal ARF.

ARF due to Pre-renal Azotemia

There were several etiological factors responsible for ARF in this group, which included 60 patients; 24 patients at the Islamic Hospital, 19 patients at Jordan University Hospital and 17 at Jordan Hospital. Volume depletion due to either diuretic abuse or gastrointestinal fluid losses was responsible for 23 cases (38.3%). Renal hypoperfusion due to cardiac disease (myo­cardial infarction, congestive heart failure, and cardiac tamponade) in 20 cases (33.3%). The use of hypotensive drugs, including angiotensin-converting enzyme (ACE-inhi­bitors), was responsible for reversible ARF in 10 patients (16.6%). Finally, hepatorenal syndrome (HRS) was seen in seven patients (11.6%).

Fifty-four patients (90%) were oliguric at presentation, of whom four required dialysis. Recovery of kidney function was achieved in 50 patients (83%). Ten patients (17%) died, including seven due to HRS.

Post-renal "ARF"

This group included 30 patients (14%); 15 at Jordan Hospital, nine patients at Jordan University Hospital, and six at the Islamic Hospital. Stones were responsible for 12 cases (40%), bladder neck obstruction for 10 cases (33.3%), retroperitoneal fibrosis for seven (23.3%), and ligation of the ureters in a horseshoe kidney in one patient (3.3%). Oligo-anuria was seen in 18 patients; five of them had solitary kidneys. Six patients required dialysis. Recovery was achieved in 28 patients. Two patients died; both were females with advanced pelvic malignant diseases. Temporary percutaneous nephrostomies were inserted in eight patients prior to surgical intervention. Five patients with retroperitoneal fibrosis required insertion of ureteric stents with good recovery of renal function.

ARF due to Renal Parenchymal Diseases

A total of 125 cases were seen in this group (58%), 48 cases at Jordan Hospital, 42 cases at the Islamic Hospital, and 35 cases at Jordan University Hospital. Acute tubular necrosis (ATN) was the cause in 70 Cases (56%), followed by glomerulonephritis/ vasculitis in 20 cases (16%), acute interstitial nephritis "AIN" in 18 cases (14.4%), tumor lysis syndrome in eight cases (6.4%) pregnancy related ARF in five cases (4%), and renal failure associated with hypercalcemia in four cases (3.2%). Acute interstitial nephritis "AIN" of different etiologies was seen 18 patients; eight were secondary to NSAID, three due to cephalosporine anti­biotics, two due to Allopurinol, and one was due to Rifampicin. The remaining four cases were secondary to viral acute interstitial nephritis. In this group, twelve of the 18 patients were oliguric, and kidney biopsies were performed in six of them. Nine patients received steroids with excellent response and decline in serum creatinine. Two out of the 18 patients required dialysis.

Eighty patients in this group were oligo­anuric (64%) and 45 patients were non­oliguric (36%). Among the 70 patients with ATN, the different etiological factors are shown in [Table - 1].

Ischemic ATN in association with septic shock and/or major cardio-vascular surgery was the most frequent cause of ATN.

Complete recovery of renal function was observed in 85 patients (68%), partial recovery in ten patients (8%), while 30 patients (24%) showed no functional recovery. Thirty patients (24%) required dialysis of whom 24 were oligo-anuric. Thirty-five patients (28%) died in this group; 26 were oliguric. Both sepsis and cardiac causes were responsible for nearly 75% of the deaths.


   Discussion Top


In this study, the spectrum of the different etiological factors for ARF was not different from what has been published previously [12],[13],[14],[15] . ARF of renal type was seen in the majority of patients. Obstructive uropathy causing ARF came second (14%), and nearly 50% of these were seen at one hospital (Jordan Hospital). Previous reports from Jordan showed that only 2% of hospital acquired ARF was due to obstruction [16] . The explanation for this may be because most of our patients were from other Arab countries (Yemen, Sudan) known to have high incidence of renal stones.

In our study, patients with ATN secondary to ischemia or nephrotoxicity formed the largest group. This is mostly iatrogenic and preventable [17] . This can be achieved by proper attention to both intra-operative and postoperative hemodynamic status of the patients, proper choice and adjustment of antibiotics' dosage [18] .

Contrast nephropathy (CN) was seen in 15 patients following a variety of radiological procedures, including cardiac catheterization, CT scans of different organs, angiography, venography and intravenous urography. Most of these patients were elderly, diabetics and had some degree of renal functional impair­ment. All of these are known risk factors for developing contrast nephropathy [19],[20] . This form of ARF can be prevented by careful identification of patients at risk, good hydration with normal saline prior to the administration of the contrast, and the use of calcium channel blocking agents [20],[21] . Recent studies did not show significant benefit of the use of non-ionic contrast over the ionic compounds in the prevention of CN [22] .

Acute interstitial nephritis "AIN" of different etiologies was seen and their presentations as well as their outcome were comparable to previously published reports [23],[24],[25],[26],[27] .

The overall survival of our patients was (80.5%). However, some subgroups, such as those with HRS and ARF secondary to renal parenchymal disease had worse prognosis. The first hand on management by the nephrologist might have contributed to the better outcome in our patients as has been reported elsewhere [28] .

In conclusion, we presented here our experience with ARF in Jordan, and it is in agreement to what has been published in the field, especially that oliguria at the onset of ARF carries a high morbidity and mortality rate. We emphasize that early referral of critically ill ARF patients to the nephrologist may significantly improve the outcome.

 
   References Top

1.Corwin HL, Bonventre JV. Acute renal failure. Medical Chn North Am 1986;70 (5): 1037-54.  Back to cited text no. 1    
2.Schricr RW. Burke TJ. New aspects in pathogenesis of acute renal failure. Nephrol Dial Transplant 1994;9(Suppl 4):9-14.  Back to cited text no. 2    
3.Flamenbaum W, Kaufman JS. Acute renal failure. The Kidney 1976;9(5):21-6.  Back to cited text no. 3    
4.Groeneveld ABS Tran DD, van-der Meulen J,Nauta JJ, Thijs LG. Acute renal failure in the medical intensive care unit: predisposing, complicating factors and outcome. Ncphron 1991;59(4):602-10.  Back to cited text no. 4    
5.Coscntmo F, Chaff C, Piedmonte M. Risk factors influencing survival in. ICU acute renal failure. Nephrol Dial Transplant 1994;9(Suppl4):179-82.  Back to cited text no. 5    
6.Schaefer JH, Jochimsen F, Keller F, Wegscheider K. Distler A. Outcome prediction of acute renal failure in medical intensive care. Intensive Care Med 1991; 17:19-24.  Back to cited text no. 6    
7.Stott RB, Cameron JS, Ogg CS, Bewick M.Why the persistently high mortality in acute renal failure? Lancet 1972;2:75-9.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
8.Anderson RJ, Linas SL, Bern AS, et al. Nonoliguric acute renal failure. N Engl J Med 1977;296:1134-8.  Back to cited text no. 8    
9.Meyers C, Rose DM, Hano JE. The clinical course of nonoliguric acute renal failure. Cardio-Vascular Medicine 1977;2(7):669-72.  Back to cited text no. 9    
10.Ledigham JG. Acute renal failure: etiology. The Islamic World Med J 1984;1(6):18-21.  Back to cited text no. 10    
11.Cameron JS. Acute renal failure in the intensive care unit today. Intensive Care Med 1986;12:64-70.  Back to cited text no. 11  [PUBMED]  
12.Jha V, MalhotraHS, Sakhuja V, Chugh KS. Spectrum of hospital-acquired acute renal failure in the developing countries Chandigarh study. Q J Med 1992;83(303): 497-505.  Back to cited text no. 12    
13.Hou SH, Bushinsky DA, Wish JB, Cohen JJ, Harrington JT. Hospital acquired renal insufficiency: a prospective study. Am J Med 1983;74:243-8.  Back to cited text no. 13  [PUBMED]  
14.Said R, Said S. Acute renal failure in Saudi Arabia. (Retrospective analysis of 100 cases). Dirasat 1988;15(4):124-35.  Back to cited text no. 14    
15.Beaman M, Turney JH, Rodger RS,. McGomglc RS ? Adu D, Michael I Changing pattern of acute renal failure. Q J Med 1987;62:15-23.  Back to cited text no. 15    
16.El-Lozi M? Akash N, Gneimat M, et al. Hospital acquired acute renal failure. Saudi J Kidney Dis Transplant l996;7(4):378-82.  Back to cited text no. 16    
17.Wagner K, Daul A. Prevention of acute renal failure. Med Klin 1993;88:251-5.  Back to cited text no. 17    
18.Appel GB. Aminoglycoside nephrotoxicity. AmJMedl990;88:16S-20S.  Back to cited text no. 18    
19.Parfrey PS, Griffiths SM, Barrett BJ; et al. Contrast material induced renal failure in patients with diabetes mellitus, renal insufficiency, or both. N Engl J Med 1989;320:143-9.  Back to cited text no. 19    
20.Porter GA. Radiocontrast-induced nephropathy. Nephrol Dial Transplant 1994;9 (Suppl 4): 146-56.  Back to cited text no. 20  [PUBMED]  
21.Neumayer HH Junge W, Kufher A, Wenning A. Prevention of radio­contrastmedia induce nephrotoxity by the calcium channel blocker nitrendipine: a prospective randomized clinical trial. Nephrol Dial Transplant 1989;4:1030-6.  Back to cited text no. 21    
22.Schwab SJ, Hlatky MA, Pieper KS, et al. Contrast nephrotoxicity: a randomized controlled trial of a nonionic and an ionic radiographic contrast agents. N Engl J Med 1989;320:149-53.  Back to cited text no. 22  [PUBMED]  
23.Lmton Al, Clark WF, Driedger AA, TurnbuII DI, Lindsay RM. Acute interstitial nephritis due to drugs: review of the literature with a report of nine cases. Ann IntMed 1980:93:735-41.  Back to cited text no. 23    
24.Cameron JS. Allergic interstitial nephritis:clinical features and pathogencsis. Q J Med 1988;66:97-115.  Back to cited text no. 24  [PUBMED]  [FULLTEXT]
25.Schlondorff D. Renal complications of nonsteroidal anti-iriflammatory drugs. Kidney Int 1993:44:643-53.  Back to cited text no. 25    
26.Unsworth J, Sturman S, Lunec J, Blake DR. Renal impairment associated with nonsteroidal anti-inflammatory drugs. J Rheum Dis 1989;46:233-6.  Back to cited text no. 26    
27.Utas C, Gulmez I: Kelestimur F, Demir R, Yucesoy M, Ozesmi M. Acute renal failure due to rifampicin treatment. Nephron 1994:67{3):367-8.  Back to cited text no. 27    
28.Mehta R, Farkas A, Pascual M, Fowler W. Effect of delayed consultation on outcome form acute renal failure in ICU. J Am Soc Nephrol 1995;6:471.  Back to cited text no. 28    

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Correspondence Address:
Riyad Said
Department of Medicine, Jordan Hospital, P.O. Box 520248, Amman
Jordan
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PMID: 18408305

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