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Saudi Journal of Kidney Diseases and Transplantation
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EDITORIAL Table of Contents   
Year : 2006  |  Volume : 17  |  Issue : 3  |  Page : 316-319
The Renal Allograft Donor with Isolated Microhematuria


Kanoo Kidney Centre, Dammam Central Hospital, Dammam, Saudi Arabia

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   Abstract 

Recently, there has been extensive debate about extending the criteria for accepting living donors to include the presence of mild renal abnormalities such as isolated microhematuria. Hematuria defined as the detection of greater than five red blood cells per high power field can be associated with abnormalities throughout the urinary tract. Detection of casts or dysmorphic red blood cells in the urine sediment with or without proteinuria could indicate underlying intrinsic renal disease. Anatomic causes, such as stones and tumors, should be excluded; cystoscopy may be indicated to exclude bladder pathology. Obviously, urinary tract infection, uncontrolled hypertension and latent diabetes mellitus must be excluded. Microscopic hematuria could be associated with mesangial IgA deposits; as 10% of first-degree relatives of patients with IgA glomerulonephritis suffer from microhematuria and/or proteinuria that may require consideration of renal biopsy. Microhematuria could also be associated with other known hereditary renal diseases such as C3 deposits disease, IgM nephropathy, autosomal dominant polycystic kidney disease, Alport's syndrome or thin basement membrane disease. In conclusion, careful assessment of isolated microhematuria, in the context of living kidney donation, is mandatory as results may reveal occult renal disease that may contraindicate kidney donation.

Keywords: Microhematuria, Kidney transplantation, Live donor.

How to cite this article:
Karkar A. The Renal Allograft Donor with Isolated Microhematuria. Saudi J Kidney Dis Transpl 2006;17:316-9

How to cite this URL:
Karkar A. The Renal Allograft Donor with Isolated Microhematuria. Saudi J Kidney Dis Transpl [serial online] 2006 [cited 2019 Nov 17];17:316-9. Available from: http://www.sjkdt.org/text.asp?2006/17/3/316/35762

   Introduction Top


There is a worldwide progressive increase in the number of patients with end-stage renal failure (ESRD) who require renal transplant­ation. [1],[2] This trend has forced many renal transplantation programs to recruit more living and cadaveric donors.

There is still a preference for living relative to cadaveric donors due to the longer half-life of renal allografts. The shortage of deceased renal allografts has enhanced living renal transplantation. Furthermore, the long-term stability of the remaining kidney in living donors, and their normal quality of life has resulted in increased popularity of living renal allograft transplantation worldwide such as in Scandinavia and USA. [3],[4],[5] In Saudi Arabia, more than 3000 living related donor renal transplants have been performed in 13 active kidney transplant centers since 1979. [2]

However, uninephrectomy in living related donors might accelerate progression of pre­existing primary renal disease. Therefore, it is vital to carefully screen the potential donors, and to balance the risk of potential damage to the donor before transplantation is consi­dered. Recently, there has been extensive debate in the transplant literature as well as in transplantation meetings about extending the criteria for accepting living related donors with mild isolated renal abnormalities such as microhematuria. [6]

Microhematuria defined as greater than five red blood cells per high power field can be associated with abnormalities throughout the urinary tract. The term isolated microhematuria indicates that there are no other associated clinical or laboratory manifestations of kidney disease. Therefore, it is mandatory to thoroughly evaluate (by full history, clinical exami­nation and detailed laboratory and imaging studies) the potential kidney donor before a decision of kidney donation can be made.


   Evaluation of a Living Donor with Isolated Microhematuria Top


A full history and detailed clinical exami­nation are essential in ruling out any here­ditary or acquired renal diseases. Repeated examination of urinary sediment for casts or dysmorphic red blood cells with or without proteinuria may reveal underlying intrinsic renal disease. Urine culture is required to exclude the possibility of a urinary tract infection. Renal functions should be assessed by simple measurement of blood biochemistry including urea, creatinine, uric acid, electrolytes and 24-hour urine collection for creatinine clearance and proteinuria. General and immuno­logical laboratory tests such as fasting blood sugar, full blood count and immunological profile should be performed to rule out the possibilities of systemic diseases such as latent diabetes mellitus and immunological diseases that can affect the kidneys.

Anatomic causes of the urinary tract, such as stones and tumors, should be excluded by appropriate imaging techniques including intravenous urography, computerized tomo­graphy scan and magnetic resonance imaging; cystoscopy and retrograde urography may be indicated to exclude urethral and bladder pathology.

In the absence of any specific abnormalities, occult primary renal disease is still not uncommon. Microscopic hematuria can be associated with mesangial IgA deposits; as 10% of first-degree relatives of patients with IgA glomerulonephritis suffer from micro­hematuria and/or proteinuria. [7] In fact, the risk of ESRD will be greater if there is a history of renal disease, such as IgA glomerulonephritis, in first- or second-degree relatives. [8],[9] Accord­ingly, a renal biopsy may be required even in the absence of other abnormal urinary findings. Microhematuria could also be associated with other known hereditary renal diseases such as autosomal dominant polycystic kidney disease (ADPKD), Alport's syndrome and thin basement membrane disease. The diagnostic criteria used to recognize ADPKD is more than four renal cysts by ultrasonography at age 30 years. [10] Alport's syndrome should be suspected in any member of an Alport family with hematuria and/or proteinuria, ocular abnormalities or deafness. Exclusion of the diagnosis will require a renal biopsy with careful examination of the tissue by electron microscopy. [11]

While extending the criteria for accepting living donors to include donors with isolated microhematuria may be desirable to address the increasing demand on renal allografts, one should not forget that there are multiple hereditary and acquired causes of isolated microhematuria; some of which are progre­ssive in nature and may affect the remaining kidney in the living donor.

Sobh et al [12] investigated thirty potential living related kidney donors with asympto­matic microscopic hematuria of non-surgical causes. They underwent thorough history, medical and ENT examination, laboratory and radiological assessment and pure-tone audiometry. Family members were also subjected to urine analysis and audiometry. In addition, the 30 donors were subjected to kidney biopsies, which were examined by light microscopy, direct and indirect immuno­fluorescent examination and electron micro­scopy. The results showed that hereditary nephritis (with or without sensorineural deafness) was found to be the most common cause of asymptomatic microscopic hematuria (25/30), followed by isolated C3 deposits disease (3/30), IgA nephropathy (1/30) and IgM nephropathy (1/30). This clearly shows that isolated microhematuria could be a misleading term, as all 30 potential donors had obscured causes that were detected by renal biopsy. Furthermore, as a result of the progressive nature of these, the authors concluded that relatives of uremic patients with asymptomatic microscopic hematuria should not be considered for kidney donation.

In conclusion, despite the progressive increase in the number of patients with ESRD in need of living related kidneys and the opinion of extending the criteria for accepting living related donors to include mild renal abnor­malities such as microhematuria, thorough evaluation is mandatory for patients with isolated microscopic hematuria before uni­nephrectomy is considered. Isolated micro­hematuria may not be associated with other signs and symptoms or apparent clinical disease, but may, nevertheless, indicate underlying occult progressive renal disease, which contra-indicates kidney donation.

 
   References Top

1.Sommerer C, Wiesel M, Schweitzer­Rothers J, Ritz E, Zeier M. The living kidney donor: giving life, avoiding harm. Nephrol Dial Transplant 2003;18:23-6.  Back to cited text no. 1  [PUBMED]  [FULLTEXT]
2.Saudi Center for Organ Transplantation Annual Report 2004.  Back to cited text no. 2    
3.Sobh M, Nabeeh A, el-Din AS, et al. Long­term follow-up of the remaining kidney in living related kidney donors. Int Urol Nephrol 1989;21(5):547-53.  Back to cited text no. 3    
4.Chen CH, Chen Y, Chiang YJ, Wu CT, Chen HW, Chu SH. Risks and quality-of­life changes in living kidney donors. Transplant Proc 2004;36(7):1920-1.  Back to cited text no. 4    
5.Ellison MD, McBride MA, Taranto SE, Delmonico FL, Kauffman HM. Living renal donation: when transplant donors become transplant candidate. Am J Transplant 2002;2 Suppl 3:351.  Back to cited text no. 5    
6.Cohen B, Smith JM, Haase B, Persijn G, Vanrenterghem Y, Frei U. Expanding the donor pool to increase renal transplantation. Nephrol Dial Transplant 20:34-41, 2004.  Back to cited text no. 6    
7.Rambausek M, Hartz G, Waldherr R, Andrassy K, Ritz E. Familial glomerulo­nephritis. Pediatr Nephrol 1987;1:416-8.  Back to cited text no. 7  [PUBMED]  
8.Lei HH, Perneger TV, Klag MJ, Whelton PK, Coresh J. Familial aggregation of renal disease in a population-based case-control study. J Am Soc Nephrol 1998;9:1270-76.  Back to cited text no. 8  [PUBMED]  
9.Schena FP, Cerullo G, Rossini M, Lanzilotta SG, D'Altri C, Manno C. Increased risk of end-stage renal disease in familial IgA nephropathy. J Am Soc Nephrol 2002;13:453-60.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Demetriou K, Tziakouri C, Anninou K, et al. Autosomal dominant polycystic kidney disease type 2. Ultrasound, genetic and clinical correlations. Nephrol Dial Transplant 2000;15:205-11.  Back to cited text no. 10    
11.Pirson Y. Making the diagnosis of Alport's syndrome. Kidney Int 1999;56:760-75.  Back to cited text no. 11  [PUBMED]  [FULLTEXT]
12.Sobh MA, Moustafa FE, el-Din Saleh MA, Tawfik A, Ghoneim MA. Study of asymptomatic microscopic hematuria in potential living related kidney donors. Nephron 1993;65(2):190-5.  Back to cited text no. 12    

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Correspondence Address:
Ayman Karkar
Kanoo Kidney Centre, Dammam Central Hospital, PO Box 11825, Dammam 31463
Saudi Arabia
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PMID: 16970250

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