Scand J Urol Nephrol26: 409-4 12, 1992
ElFFECTS OF SCHISTOSOMIASIS ON LIVING KIDNEY DONORS Mohained A. Sobh, Salah EL-Din EL Sharkawy, Ahmed A. Shokeir, Fatma E. Moustafa, Assem K. EL Sherif and Mohamed A. Ghoneim From the Urology and Nephrology Center, University of Mansoura, Egypt
Scand J Urol Nephrol Downloaded from informahealthcare.com by Nyu Medical Center on 11/11/14 For personal use only.
(Submitted May 17, 1991. Accepted for publication November 17, 1991)
Abstract. Twenty living kidney donors with schistosomiasis were compared with 20 uninfected donors for a mean follow-up period of 42 months (range 12-62). All patients with schistosomiasis had been treated preoperatively with antischistosomal chemotherapy. None of the donors developed any appreciable change in mean syslolic or diastolic blood pressure during the follow-up period, though one infected and two uninfected donors had traces of protein in the urine. One uninfected donor developed microscopic haematuria. The two groups has similar reductions in renal function after unilateral nephrectomy. The response of the remaining kidneys to a combined infusion of dopamine and an amino acid preparation was similar in both groups. One infected and two uninfected donors were found to have devloped mild hydroureter and hydronephrosis on excretory urography. Schistosomiasis did not significantly affect compensatory hypertrophy of the remaining kidney. We conclude that uncomplicaled schistosomiasis in living kidney donors does not adversely affect either the function or the morphology of the remaining kidney, at least during an observation period of up to five years. Schistosomal infection does not seem to alter the adaptive changes in 1 he remaining kidney, provided that the donor had functionally and morphologically intact kidneys and that the schistosomiasis was treated before kidney donation. Longer term evaluation is recommended, however, to confirm the validity of these observations. Key words: schistosomiasis, kidney transplantation, kidney donor, kidney reserve.
Schistosomiasis affects 200 to 350 million people, mainly in tropical and subtropical areas (1). Schistosoma haematobium may lead to the development of a variety of irreversible pathological changes in the urinary tract (4), and there is an association between Schistosoma mansoni and glomerulopathy. This was initially thought to be circumstantial, but experimental and clinical studies have confirmed its existence (1-14).
The impact of schistosomiasis on renal transplant recipients has been reported by many investigators (2, 7, 20), but the effect of the disease on living kidney donors is still uncertain. The aim of this study was to investigate such effects. PATIENTS AND METHODS Patients Forty living kidney donors took part in this study. Twenty donors had definite schistosomiasis (group I ) and the other 20 were free of schistosomal infection (group 11); the two groups were matched for age and sex distribution. Detection of schistosomiasis A history of infection or treatment was elicited. Three urine and stool specimens were analysed for schistosomal ova and occult blood. Serum indirect schistosomal haemagglutination titres were measured. All donors in whom stool analysis and haemagglutination test failed to show the presence of infection underwent biopsy of the rectal mucosa to see if there were any sings of egg deposits or schistosomal granulomas o r both. An intraoperative ureteric biopsy specimen was taken from every donor and examined histopathologically for presence of egg deposits, granuloma, and associated mucosal changes. Mucosal changes expected to be seen in schistosomal patients are Brunn’s nests, ureteritis glandularies, ureteritis cystica, or squamous metablasia. Evaluation before nephrectomy All kidney donors had an intravenous urogram, ultrasound examination, and measurement of serum creatinine concentration and creatinine clearance before nephrectomy. As a routine, kidney donors were excluded if any abnormality in renal function or any radiological evidence of disease of the urinary tract was discovered. All participants with schistosomal infections were treated with 60 mg/kg praziquantel given in two divided doses on the same day, together with 60 mg/kg oxamniquine. 20 mg on each of three consecutive days. Scand J Urol Nephrol26
410
M. A . Sobh et al.
Table I. Renal function before and after unilateral nephrectomy in infected and uninfected donors
Scand J Urol Nephrol Downloaded from informahealthcare.com by Nyu Medical Center on 11/11/14 For personal use only.
Group 1 (Infected donors) Group I1 (Uninfected donors)
Mean (SD) serum creatinine (pmolll)
Mean (SD) creatinine clearance (ml/min)
Before nephrectomy
After nephrectomy
Before nephrectomy
After nephrectomy
64.0 (21.3)
94.2 (17.8)
O.OOOl* 0.17**
138.1 (26.22)
84.15 (21.63)
O.OOOl* 0.43**
65.8 (16.0)
92.5 (13.3)
0.0001*
127.8 (16.83)
83.7 (16.83)
0.0001*
p-Value
p-Value
Comparisons before and after nephrectomy were made with the sign test*, and those between the two groups with the Mann Whitney test**.
Assessment afer nephrectomy At the time of entry into the study, donors in both groups were assessed by urine analysis, urography and ultrasonography of the remaining kidney. Glomerular filtration rate (GFR) was measured both by 99mTc diethylenetriaminepenta-acetic acid (DPTA) scans and by the measurement of 24 hour endogenous creatinine clearance. The functional reserve of the remaining kidney was then assessed by simultaneous infusion of dopamine (2.5 pg/kg/min) and 10°/o solution of the multiamino acid preparation Vamin N@ (80 ml/hour) for 12 hours. During the procedure a diuresis of at least 100 ml/hour was maintained with oral fluids. After six hours of combined dopamine and amino acid infusion, when the GFR has reached its maximum, isotope clearance was measured by 9 9 m TDTPA ~ scans. Urine was also collected and endogenous creatinine clearance was measured after 12 hours. The functional reserve of the remaining kidney was assessed by comparing the clearance values on both isotope and chemical tests, with the corresponding values measured before the infusion of dopamine and amino acids.
RESULTS Twenty donors with schistosomiasis (group I) and 20 uninfected donors (group 11) took part in the study. Of the infected donors, 8 has S. mansoni and 12 had S. mansoni and S. haematobium infections. S, mansoni eggs were detected in the stools of eight donors and in the rectal mucosal biopsy specimens of 13 donors. S. haematobium eggs with or without mucosal changes were found in the ureteric biopsy specimens of eight donors. In four donors schistosomiasis was diagnosed from a combination of history and high schistosomal haemagglutination titres. Uninfected donors had no history of exposure to infection and had negative results for all tests. The mean follow-up period after donation was 42 months (range 12-62). None of the donors developed any appreciable change in the
Table 11. Eflect of infusion of dopamine and amino acids on GFR (mllmin) in infected and uninfected donors after unilateral nephrectomy Mean (SD) GFR estimated by isotope clearance
Mean (SD) G F R estimated by creatinine clearance
Basal value Group I (Infected donors) Group I1 (Uninfected donors)
84.15 (21.63) 83.7 (16.83)
&and J Urol Nephrol26
Value after infusion
98 (21.69) 104 (32.1)
Kidney reserve
Kidney reserve
(Yo)
Basal value
Value after infusion
18.36 (15.48)
65.5 (7.54)
73.25 (6.78)
12.94 (15.06)
24.53 (22.15)
67.5 (1 1.9)
75.15 (8.77)
13.07 (15.33)
(W
Scand J Urol Nephrol Downloaded from informahealthcare.com by Nyu Medical Center on 11/11/14 For personal use only.
Esfects of schistosorniasis on living kidney donors mean systolic or diastolic blood pressure. Urine analysis showed that one infected and two uninfected donors had traces of protein in the urine, and one uninfected donor had microscopic haematuria. Both groups had a significant reduction in total renal function after unilateral nephrectomy (Table I), but the reduction was similar in the two groups. Serum creatinine concentrations increased by 37% and 41 O/o in infected and uninfected donors respectively. Creatinine clearance decreased by 39 Yo and 35 Yo from the basal values, but when the creatinine clearance of the remaining kidney was compared with half the corresponding predonation values, it had increased by 22% and 31 % respectively. Infusion of dopamine and amino acids significantly increased the GFR in both groups (Table 11). The response to the infusion was comparable in infected and uninfected donors. Three of the 40 donors had abnormalities on urography. One infected donor developed mild hydroureter and hydronephrosis five years after unilateral nephrectomy because of senile enlargement of the prostate. An uninfected female donor had mild dilatation of the pelvicalyceal system four months after delivery. Another uninfected donor developed an unexplained stricture of the pelvic part of the remaining ureter three years after unilateral nephrectomy. Seventeen of all the donors (3%) had increases in the size of their remaining kidneys, but there was no significant difference between the infected and the uninfected donors. DISCUSSION We know of only a single report on the outcome of living kidney donors with schistosomiasis (7), in which 12 living kidney donors were described to have schistosomiasis before unilateral nephrectomy. The authors recommended that potential donors who show any evidence of structural changes should be excluded from donation, even if only small sandy patches are seen on cystoscopy. In our study, neither group had any evidence of changes in mean systolic or diastolic blood pressure during the follow-up period. A high incidence of hypertension after donation (6.7%) was reported by Najarian et al. (11)
41 1
whereas Sutherland et al. (15) showed that the incidence was not higher than that in the general population. Characteristics of the investigated donors varied greatly from one study to another, however, in the present study, the mean (SD) age of donors was 35 (1 9) years, which is lower than that in most of the other reported studies of uninfected donors. Isolated proteinuria (trace to one plus) was found in one case ( 5 % ) of our infected group and in two of the uninfected cases (10%). The development of proteinuria in kidney donors has been explained by the increased permeability of the capillary wall to plasma protein induced by hyperfiltration (16). Vincenti et al. (1 9) found no correlation between protein excretion in urine and length of time after unilateral nephrectomy. Variations in response to hyperfiltration have, however, been documented in several studies (12-1 3). Microscopic haematuria was found in only one of our uninfected donors, and was reported again after donation; this was explained by change in renal haemodynamics, morphological alterations, and increased glomerular permeability ( 5 ) . The low incidence of urinary abnormalities in either group of donors renders it difficult to make inferences about the possible impact of schistosomiasis on the dynamics of renal blood flow or on the integrity of glomerular filtration. A comparable decline in renal function after unilateral nephrectomy was detected in both groups of donors. However, such a decline did not reduce kidney function outside the limits of the reference range. Moreover, the response of the remaining kidney to infusion of dopamine and amino acids was similar in infected and uninfected donors; both groups had significant increases in GFR. The estimated mean functional reserve of all donors was 13 %, which was similar to that of Bosch et al. (3) and greater than that of Tapson et al. (1 7). Three of our 40 donors had abnormal changes on urography as a result of causes not apparently related to schistosomiasis. Of the 12 infected donors investigated by Hefty & McCorkell (7), only one had slight progression of pre-existing distal ureteric dilatation. These findings may be impossible to substantiate until there has been a longer follow-up of more infected and uninfected donors. Scand J Urol Nephrof 26
Scand J Urol Nephrol Downloaded from informahealthcare.com by Nyu Medical Center on 11/11/14 For personal use only.
412
M. A . Sobh et al.
Schistosomiasis did not significantly affect the compensatory hypertrophy of the remaining kidney; 17 (43 Yo) of our donors had appreciable increases in the size of their kidneys. Traditionally, this increase especially in length of the kidney was explained by cellular hypertrophy and hyperplasia (8-1 8). The most impressive changes were found in the proximal convoluted tubules, which had definitely increased in both diameter and length (6). The exact mechanisms of compensatory hypertrophy and hyperplasia are not clear, but, the increased work load on the remaining kidney (9) and the relase of humoral renotrophic factors (10) were the most wildly accepted. In our study there were 22% and 3 1 Yo increases in the endogenous creatinine clearance of the remaining kidney in infected and uninfected donors, respectively. The implications of our results are important, as schistosomiasis is common in Egypt and in many other countries where kidney transplantation is largely dependent on the availability of living related donors. Results indicate that uncomplicated schistosomiasis of living kidney donors does not adversely affect either the function or the morphology of the remaining kidney, at least during the reported period of follow-up (1-5 years). Schistosomal infection does not seem to alter the adaptive changes in the remaining kidney, provided that the donor had functionally and morphologically intact kidneys and that schistosomiasis was treated before the kidney was donated. Nevertheless, longer term evaluation is recommended to confirm these findings. ACKNOWLEDGEMENT We thank Miss Alyaa Radwan for typing the manuscript.
REFERENCES 1 . Andrade ZA, Rocha H. Schistosomal glomerulopathy. Kidney Int 1979; 16: 23-29. 2. Azevedo LS. De Paula FJ, Ianhez LE et al. Renal transplantation and schistosomiasis mansoni. Transplantation 1987; 44: 795-798. 3. Bosch JP, Lauer A, Glabman S. Short term protein loading in assessment of patients with renal disease. Am J Med 1984; 7: 873-879. 4. Ghoneim MA: Bilharziasis. The lower genitourinary tract. In: Husain J, ed. Tropical urology and Scand J Urol Nephrol26
5.
6. 7.
8. 9.
10.
I. 2.
3.
14.
15.
16. 17. 18.
19. 20.
renal disease. Edinburgh: Churchill Livingstone, 1984: 261-280. Hakim RM, Goldszer RC, Brenner B. Hypertension and proteinuria: Long term sequelae of uninephrectomy in humans. Kidney Int 1984; 25: 930-936. Hayslett JP, Kashgariar M Epstein FH. Functional correlates of compensatory renal hypertrophy. J Clin Invest 1968; 47: 774-782. Hefty TR, McCorkell SJ. Schistosomiasis and renal transplantation. J Urol 1986; 135: 1 163-1 166. Johnson HA, Vera Roman JM. Compensatory renal enlargement. Hypertrophy versus hyperplasia. Am J Pathol 1960; 49: 1-13. Katz AL. Renal function immediately after contralateral nephrectomy. Relation to the mechansim of compensatory kidney growth. Yale J Biol Med 1970; 43: 164-169. Lyons HJ, Evan AP, McLaren LC, Soloman S. In vitro evidence for a renotrophic factor in renal compensatory hypertrophy. Nephron 1974; 13: 198-204. Najarian JS, Weilland D , Chavers B et al. Studies on living related kidney donors at single institution. Proc EDTA 1984; 21: 91 1-919. Piet M, Wee T , Geerlings W, Rosman JB, Sluiter W, Geest S, Donker A. Testing renal reserve filtration capacity with an amino acid solution. Nephron 1985; 41: 193-199. Rodriguez-lturbe B, Herrera J, Gracia R. Response to acute protein load in kidney donors and in apparently normal post-acute glomerulonephritis: Evidence for glomerular hyperfiltration. Lancet 1985; 31 August 8453: 461-464. Sobh MA, Moustafa FE, Sally SM et al. Characterization of kidney lesions in early schistosomalspecific nephropathy. Nephrol Dial Transplant 1988; 3: 392-398. Sutherland DER, Goetz FC, Kendall DM, Najarian JS. Effect of donor source, technique, immunosuppression and presence or absence of endstage diabetic nephropathy on outcome in pancreas transplant recipients. Trans Proc 1985; 17: 325-327. Tapson JS, Marshall SM, Tisdall SR et al. Renal function and blood pressure after donor nephrectomy. Proc EDTA 1984; 21: 580-587. Tapson JS, Mansy H, Marshall SM. Renal functional reserve in kidney donors. Q J Med 1986; 60: 725-732. Therfall G , Taylor DM, Buck AT. Studies of the changes in growth and DNA synthesis in the rat kidney during experimentally induced renal hypertrophy. Am J Pathol 1967; 5: 14-19. Vincenti F, Amend WJC, Kaysen G et al. Longterm renal function in kidney donors. Transplantation 1983; 36: 626-629. Weeden D, Hopwell JP, Morehead JF et al. Schistosomiasis in renal transplantation. Br J Urol 1982; 54: 478-479.
ElFFECTS OF SCHISTOSOMIASIS ON LIVING KIDNEY DONORS Mohained A. Sobh, Salah EL-Din EL Sharkawy, Ahmed A. Shokeir, Fatma E. Moustafa, Assem K. EL Sherif and Mohamed A. Ghoneim From the Urology and Nephrology Center, University of Mansoura, Egypt
Scand J Urol Nephrol Downloaded from informahealthcare.com by Nyu Medical Center on 11/11/14 For personal use only.
(Submitted May 17, 1991. Accepted for publication November 17, 1991)
Abstract. Twenty living kidney donors with schistosomiasis were compared with 20 uninfected donors for a mean follow-up period of 42 months (range 12-62). All patients with schistosomiasis had been treated preoperatively with antischistosomal chemotherapy. None of the donors developed any appreciable change in mean syslolic or diastolic blood pressure during the follow-up period, though one infected and two uninfected donors had traces of protein in the urine. One uninfected donor developed microscopic haematuria. The two groups has similar reductions in renal function after unilateral nephrectomy. The response of the remaining kidneys to a combined infusion of dopamine and an amino acid preparation was similar in both groups. One infected and two uninfected donors were found to have devloped mild hydroureter and hydronephrosis on excretory urography. Schistosomiasis did not significantly affect compensatory hypertrophy of the remaining kidney. We conclude that uncomplicaled schistosomiasis in living kidney donors does not adversely affect either the function or the morphology of the remaining kidney, at least during an observation period of up to five years. Schistosomal infection does not seem to alter the adaptive changes in 1 he remaining kidney, provided that the donor had functionally and morphologically intact kidneys and that the schistosomiasis was treated before kidney donation. Longer term evaluation is recommended, however, to confirm the validity of these observations. Key words: schistosomiasis, kidney transplantation, kidney donor, kidney reserve.
Schistosomiasis affects 200 to 350 million people, mainly in tropical and subtropical areas (1). Schistosoma haematobium may lead to the development of a variety of irreversible pathological changes in the urinary tract (4), and there is an association between Schistosoma mansoni and glomerulopathy. This was initially thought to be circumstantial, but experimental and clinical studies have confirmed its existence (1-14).
The impact of schistosomiasis on renal transplant recipients has been reported by many investigators (2, 7, 20), but the effect of the disease on living kidney donors is still uncertain. The aim of this study was to investigate such effects. PATIENTS AND METHODS Patients Forty living kidney donors took part in this study. Twenty donors had definite schistosomiasis (group I ) and the other 20 were free of schistosomal infection (group 11); the two groups were matched for age and sex distribution. Detection of schistosomiasis A history of infection or treatment was elicited. Three urine and stool specimens were analysed for schistosomal ova and occult blood. Serum indirect schistosomal haemagglutination titres were measured. All donors in whom stool analysis and haemagglutination test failed to show the presence of infection underwent biopsy of the rectal mucosa to see if there were any sings of egg deposits or schistosomal granulomas o r both. An intraoperative ureteric biopsy specimen was taken from every donor and examined histopathologically for presence of egg deposits, granuloma, and associated mucosal changes. Mucosal changes expected to be seen in schistosomal patients are Brunn’s nests, ureteritis glandularies, ureteritis cystica, or squamous metablasia. Evaluation before nephrectomy All kidney donors had an intravenous urogram, ultrasound examination, and measurement of serum creatinine concentration and creatinine clearance before nephrectomy. As a routine, kidney donors were excluded if any abnormality in renal function or any radiological evidence of disease of the urinary tract was discovered. All participants with schistosomal infections were treated with 60 mg/kg praziquantel given in two divided doses on the same day, together with 60 mg/kg oxamniquine. 20 mg on each of three consecutive days. Scand J Urol Nephrol26
410
M. A . Sobh et al.
Table I. Renal function before and after unilateral nephrectomy in infected and uninfected donors
Scand J Urol Nephrol Downloaded from informahealthcare.com by Nyu Medical Center on 11/11/14 For personal use only.
Group 1 (Infected donors) Group I1 (Uninfected donors)
Mean (SD) serum creatinine (pmolll)
Mean (SD) creatinine clearance (ml/min)
Before nephrectomy
After nephrectomy
Before nephrectomy
After nephrectomy
64.0 (21.3)
94.2 (17.8)
O.OOOl* 0.17**
138.1 (26.22)
84.15 (21.63)
O.OOOl* 0.43**
65.8 (16.0)
92.5 (13.3)
0.0001*
127.8 (16.83)
83.7 (16.83)
0.0001*
p-Value
p-Value
Comparisons before and after nephrectomy were made with the sign test*, and those between the two groups with the Mann Whitney test**.
Assessment afer nephrectomy At the time of entry into the study, donors in both groups were assessed by urine analysis, urography and ultrasonography of the remaining kidney. Glomerular filtration rate (GFR) was measured both by 99mTc diethylenetriaminepenta-acetic acid (DPTA) scans and by the measurement of 24 hour endogenous creatinine clearance. The functional reserve of the remaining kidney was then assessed by simultaneous infusion of dopamine (2.5 pg/kg/min) and 10°/o solution of the multiamino acid preparation Vamin N@ (80 ml/hour) for 12 hours. During the procedure a diuresis of at least 100 ml/hour was maintained with oral fluids. After six hours of combined dopamine and amino acid infusion, when the GFR has reached its maximum, isotope clearance was measured by 9 9 m TDTPA ~ scans. Urine was also collected and endogenous creatinine clearance was measured after 12 hours. The functional reserve of the remaining kidney was assessed by comparing the clearance values on both isotope and chemical tests, with the corresponding values measured before the infusion of dopamine and amino acids.
RESULTS Twenty donors with schistosomiasis (group I) and 20 uninfected donors (group 11) took part in the study. Of the infected donors, 8 has S. mansoni and 12 had S. mansoni and S. haematobium infections. S, mansoni eggs were detected in the stools of eight donors and in the rectal mucosal biopsy specimens of 13 donors. S. haematobium eggs with or without mucosal changes were found in the ureteric biopsy specimens of eight donors. In four donors schistosomiasis was diagnosed from a combination of history and high schistosomal haemagglutination titres. Uninfected donors had no history of exposure to infection and had negative results for all tests. The mean follow-up period after donation was 42 months (range 12-62). None of the donors developed any appreciable change in the
Table 11. Eflect of infusion of dopamine and amino acids on GFR (mllmin) in infected and uninfected donors after unilateral nephrectomy Mean (SD) GFR estimated by isotope clearance
Mean (SD) G F R estimated by creatinine clearance
Basal value Group I (Infected donors) Group I1 (Uninfected donors)
84.15 (21.63) 83.7 (16.83)
&and J Urol Nephrol26
Value after infusion
98 (21.69) 104 (32.1)
Kidney reserve
Kidney reserve
(Yo)
Basal value
Value after infusion
18.36 (15.48)
65.5 (7.54)
73.25 (6.78)
12.94 (15.06)
24.53 (22.15)
67.5 (1 1.9)
75.15 (8.77)
13.07 (15.33)
(W
Scand J Urol Nephrol Downloaded from informahealthcare.com by Nyu Medical Center on 11/11/14 For personal use only.
Esfects of schistosorniasis on living kidney donors mean systolic or diastolic blood pressure. Urine analysis showed that one infected and two uninfected donors had traces of protein in the urine, and one uninfected donor had microscopic haematuria. Both groups had a significant reduction in total renal function after unilateral nephrectomy (Table I), but the reduction was similar in the two groups. Serum creatinine concentrations increased by 37% and 41 O/o in infected and uninfected donors respectively. Creatinine clearance decreased by 39 Yo and 35 Yo from the basal values, but when the creatinine clearance of the remaining kidney was compared with half the corresponding predonation values, it had increased by 22% and 31 % respectively. Infusion of dopamine and amino acids significantly increased the GFR in both groups (Table 11). The response to the infusion was comparable in infected and uninfected donors. Three of the 40 donors had abnormalities on urography. One infected donor developed mild hydroureter and hydronephrosis five years after unilateral nephrectomy because of senile enlargement of the prostate. An uninfected female donor had mild dilatation of the pelvicalyceal system four months after delivery. Another uninfected donor developed an unexplained stricture of the pelvic part of the remaining ureter three years after unilateral nephrectomy. Seventeen of all the donors (3%) had increases in the size of their remaining kidneys, but there was no significant difference between the infected and the uninfected donors. DISCUSSION We know of only a single report on the outcome of living kidney donors with schistosomiasis (7), in which 12 living kidney donors were described to have schistosomiasis before unilateral nephrectomy. The authors recommended that potential donors who show any evidence of structural changes should be excluded from donation, even if only small sandy patches are seen on cystoscopy. In our study, neither group had any evidence of changes in mean systolic or diastolic blood pressure during the follow-up period. A high incidence of hypertension after donation (6.7%) was reported by Najarian et al. (11)
41 1
whereas Sutherland et al. (15) showed that the incidence was not higher than that in the general population. Characteristics of the investigated donors varied greatly from one study to another, however, in the present study, the mean (SD) age of donors was 35 (1 9) years, which is lower than that in most of the other reported studies of uninfected donors. Isolated proteinuria (trace to one plus) was found in one case ( 5 % ) of our infected group and in two of the uninfected cases (10%). The development of proteinuria in kidney donors has been explained by the increased permeability of the capillary wall to plasma protein induced by hyperfiltration (16). Vincenti et al. (1 9) found no correlation between protein excretion in urine and length of time after unilateral nephrectomy. Variations in response to hyperfiltration have, however, been documented in several studies (12-1 3). Microscopic haematuria was found in only one of our uninfected donors, and was reported again after donation; this was explained by change in renal haemodynamics, morphological alterations, and increased glomerular permeability ( 5 ) . The low incidence of urinary abnormalities in either group of donors renders it difficult to make inferences about the possible impact of schistosomiasis on the dynamics of renal blood flow or on the integrity of glomerular filtration. A comparable decline in renal function after unilateral nephrectomy was detected in both groups of donors. However, such a decline did not reduce kidney function outside the limits of the reference range. Moreover, the response of the remaining kidney to infusion of dopamine and amino acids was similar in infected and uninfected donors; both groups had significant increases in GFR. The estimated mean functional reserve of all donors was 13 %, which was similar to that of Bosch et al. (3) and greater than that of Tapson et al. (1 7). Three of our 40 donors had abnormal changes on urography as a result of causes not apparently related to schistosomiasis. Of the 12 infected donors investigated by Hefty & McCorkell (7), only one had slight progression of pre-existing distal ureteric dilatation. These findings may be impossible to substantiate until there has been a longer follow-up of more infected and uninfected donors. Scand J Urol Nephrof 26
Scand J Urol Nephrol Downloaded from informahealthcare.com by Nyu Medical Center on 11/11/14 For personal use only.
412
M. A . Sobh et al.
Schistosomiasis did not significantly affect the compensatory hypertrophy of the remaining kidney; 17 (43 Yo) of our donors had appreciable increases in the size of their kidneys. Traditionally, this increase especially in length of the kidney was explained by cellular hypertrophy and hyperplasia (8-1 8). The most impressive changes were found in the proximal convoluted tubules, which had definitely increased in both diameter and length (6). The exact mechanisms of compensatory hypertrophy and hyperplasia are not clear, but, the increased work load on the remaining kidney (9) and the relase of humoral renotrophic factors (10) were the most wildly accepted. In our study there were 22% and 3 1 Yo increases in the endogenous creatinine clearance of the remaining kidney in infected and uninfected donors, respectively. The implications of our results are important, as schistosomiasis is common in Egypt and in many other countries where kidney transplantation is largely dependent on the availability of living related donors. Results indicate that uncomplicated schistosomiasis of living kidney donors does not adversely affect either the function or the morphology of the remaining kidney, at least during the reported period of follow-up (1-5 years). Schistosomal infection does not seem to alter the adaptive changes in the remaining kidney, provided that the donor had functionally and morphologically intact kidneys and that schistosomiasis was treated before the kidney was donated. Nevertheless, longer term evaluation is recommended to confirm these findings. ACKNOWLEDGEMENT We thank Miss Alyaa Radwan for typing the manuscript.
REFERENCES 1 . Andrade ZA, Rocha H. Schistosomal glomerulopathy. Kidney Int 1979; 16: 23-29. 2. Azevedo LS. De Paula FJ, Ianhez LE et al. Renal transplantation and schistosomiasis mansoni. Transplantation 1987; 44: 795-798. 3. Bosch JP, Lauer A, Glabman S. Short term protein loading in assessment of patients with renal disease. Am J Med 1984; 7: 873-879. 4. Ghoneim MA: Bilharziasis. The lower genitourinary tract. In: Husain J, ed. Tropical urology and Scand J Urol Nephrol26
5.
6. 7.
8. 9.
10.
I. 2.
3.
14.
15.
16. 17. 18.
19. 20.
renal disease. Edinburgh: Churchill Livingstone, 1984: 261-280. Hakim RM, Goldszer RC, Brenner B. Hypertension and proteinuria: Long term sequelae of uninephrectomy in humans. Kidney Int 1984; 25: 930-936. Hayslett JP, Kashgariar M Epstein FH. Functional correlates of compensatory renal hypertrophy. J Clin Invest 1968; 47: 774-782. Hefty TR, McCorkell SJ. Schistosomiasis and renal transplantation. J Urol 1986; 135: 1 163-1 166. Johnson HA, Vera Roman JM. Compensatory renal enlargement. Hypertrophy versus hyperplasia. Am J Pathol 1960; 49: 1-13. Katz AL. Renal function immediately after contralateral nephrectomy. Relation to the mechansim of compensatory kidney growth. Yale J Biol Med 1970; 43: 164-169. Lyons HJ, Evan AP, McLaren LC, Soloman S. In vitro evidence for a renotrophic factor in renal compensatory hypertrophy. Nephron 1974; 13: 198-204. Najarian JS, Weilland D , Chavers B et al. Studies on living related kidney donors at single institution. Proc EDTA 1984; 21: 91 1-919. Piet M, Wee T , Geerlings W, Rosman JB, Sluiter W, Geest S, Donker A. Testing renal reserve filtration capacity with an amino acid solution. Nephron 1985; 41: 193-199. Rodriguez-lturbe B, Herrera J, Gracia R. Response to acute protein load in kidney donors and in apparently normal post-acute glomerulonephritis: Evidence for glomerular hyperfiltration. Lancet 1985; 31 August 8453: 461-464. Sobh MA, Moustafa FE, Sally SM et al. Characterization of kidney lesions in early schistosomalspecific nephropathy. Nephrol Dial Transplant 1988; 3: 392-398. Sutherland DER, Goetz FC, Kendall DM, Najarian JS. Effect of donor source, technique, immunosuppression and presence or absence of endstage diabetic nephropathy on outcome in pancreas transplant recipients. Trans Proc 1985; 17: 325-327. Tapson JS, Marshall SM, Tisdall SR et al. Renal function and blood pressure after donor nephrectomy. Proc EDTA 1984; 21: 580-587. Tapson JS, Mansy H, Marshall SM. Renal functional reserve in kidney donors. Q J Med 1986; 60: 725-732. Therfall G , Taylor DM, Buck AT. Studies of the changes in growth and DNA synthesis in the rat kidney during experimentally induced renal hypertrophy. Am J Pathol 1967; 5: 14-19. Vincenti F, Amend WJC, Kaysen G et al. Longterm renal function in kidney donors. Transplantation 1983; 36: 626-629. Weeden D, Hopwell JP, Morehead JF et al. Schistosomiasis in renal transplantation. Br J Urol 1982; 54: 478-479.
