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Volume: 19 Issue: 12 December 2021


Urolithiasis in a Deceased Donor Kidney Transplant Recipient: Case Report


Urolithiasis is a rare complication among kidney transplant recipients, with an incidence of 0.4% to 4.4%. Saudi Arabia has a very hot environment for most of the year, which has been linked to an increased incidence of nephrolithiasis. Additionally, animal protein consumption promotes stone development. Saudi Arabia has 2.5 times the number of stone formation indications as the rest of the world. Several features of urolithiasis and stone composition have already been discussed. The most frequent stone composition is calcium oxalate, followed by uric acid. We discuss the case of a 35-year-old Indian male brain death donor who presented after an automobile accident and had no history of chronic illness. One of his kidneys was transplanted into a female patient. She complained with flank pain and dysuria numerous times after transplant, which turned out to be a urinal track infection. She thereafter developed hematuria with burning micturition, and tests revealed that she had a large renal bladder stone as well as several pelvic kidney stones. The patient received lithotripsy and the stone was removed, and her kidney function was restored.

Key words : Kidney transplantation, Stone


Urolithiasis in renal transplant recipients is a rare event with an incidence ranging from 0.4% to 4.4%.1 The overall probabilities of urolith formation in renal transplant patients are variable worldwide; nevertheless, it is a global public health concern.2 Because the gap between the organ supply and the organ demand remains substantial, the need for an adequate pool of surrogates as source for healthy allografts is an ongoing critical concern.

Kidneys from extended criteria donation and donation after cardiac death are being used with greater frequency than in the past. These kidneys may be of uncertain quality and have shown a higher incidence of primary nonfunction or delayed graft function compared with standard criteria donor kidneys.3 Compared with standard criteria donation, donation after cardiac death inevitably exposes potential allografts to higher risk for hypoxia, hypotension, and inadequate organ perfusion, all of which are common during progression to circulatory arrest.

Saudi Arabia has an extremely hot climate for most of the year, and this climate is associated with the higher risk of nephrolithiasis. Furthermore, con-sumption of animal protein is high among the general population of Saudi Arabia compared with popu-lations of some other countries. These factors have been associated with an increase in urinary pH along with a consequent decrease in citrate excretion.4 High purine intake, hyperuricosuria, and acidic urine are also associated with an increased incidence of uric acid-forming stones among Saudi Arabians.

In 2001, an epidemiological study performed in Riyadh, Saudi Arabia, reported that renal calculi were 2.5 times more common in Saudi Arabia than in other countries.5 A cross-sectional study conducted from November 2018 to June 2019 at the King Abdulaziz University Hospital, Jeddah, Saudi Arabia, has shown that the prevalence of renal stones was 16.9% among the participants. Various aspects of urolithiasis and stone composition have been addressed previously in studies of various regions of Saudi Arabia. Calcium oxalate has been reported as the most common stone composition, followed by uric acid and mixed phosphates.5

A unique combination of metabolic and urodynamic factors may lead to the development of de novo allograft urolithiasis. Stone analysis has shown that calcium oxalate stones are the most common type, observed in up to 47% of the patients with allograft urolithiasis.6

The pathophysiological mechanisms include, but are not limited to, persistent hyperparathyroidism, hypercalcemia, and hyperuricemia associated with hypercalciuria and hypocitraturia.7 Renal calculi have been significantly associated with persistent urinary tract infections, notably in the development of staghorn stones in the presence of urea-splitting organisms.8-10 Surgical risk factors include ureteral obstruction, infravesical obstruction, and urinary-digestive anastomoses.11

Additionally, a few case reports have suggested other potential causes of renal calculi. It has been reported that cinacalcet treatment for posttransplant persistent hyperparathyroidism contributes to calculus formation in allografts; therefore, serum and urinary calcium should be monitored closely in these recipients.12 There is limited evidence that immunosuppressive agents, particularly cyclosporine, may also enhance stone formation.13 Rare causes for stone formation include primary hyperoxaluria type 1 (often observed with recurrent urolithiasis), nephrocalcinosis, and end-stage renal disease.14

Another rare cause for stone formation is hereditary renal hypouricemia. In a previously published case report, nephrocalcinosis diagnosed by protocol biopsy was shown to be adequately controlled with conservative measures.15 Stones may also form as a secondary symptom of forgotten ureteral stents, and shock-wave lithotripsy and laser disintegration may be required for the removal of the calcifications that may form at the site of an unretrieved stent.

Calcium-based kidney stones are the most common type observed in the general population, as well in kidney transplant recipients. Struvite stones (ammonium magnesium phosphate), also known as infected stones, are common in kidney transplant recipients (20%) than in the general population, and uric acid (10%-15%) stones are more common in kidney transplant recipients.

Shock-wave lithotripsy, flexible ureteroscopy, expectant management treatment, and open surgery may be considered as potential treatments for patients with renal stones. It is not clear whether the development of urolithiasis in the allograft would have a hazardous effect on the graft survival.10 Obviously, the rarity of the disease and the consequent difficulty to pursue an adequate analysis may be contributing factors for failure to distinguish the actual effects of the development of urolithiasis with regard to the risk for graft failure.

Here, we introduce our 55-year-old female patient, who had received a kidney transplant 10 years previous to her death. Her blood type was B positive, and her original kidney disease was recurrent pyelonephritis. She had received bladder augmentation before the kidney transplant.

Case Report

A 35-year-old Indian male donor patient presented after a motorcar accident; he had no history of chronic illness, and his blood type was B positive. The estimated ischemia time was 24 hours from bench to bedside. The posttransplant course progressed smoothly for the recipient, and she was prescribed a regimen of steroids, Myfortic (mycophenolic acid), and acceptable cyclosporine trough levels were maintained. Ten months after the transplant, she developed diabetes for which she received insulin treatment. The circumstances of the COVID-19 pandemic prevented proper follow-up with the patient.

In August 2020, she presented several times to the emergency room with flank pain and dysuria and was diagnosed with a urinary tract infection for which she received antibiotics that successfully restored stable kidney function. In January 2021, she had a severe episode of burning micturition and hematuria and was admitted to the hospital. Laboratory and imaging  investigations (Figure 1, top) were performed and revealed a large urinary bladder stone (Figure 1, bottom); lithotripsy was performed to mitigate this complication.

Several months later, in August 2020, the patient presented after an episode similar to the previous event, but with a stable kidney function. Abdominal ultrasonography showed that the urinary bladder was filled with several radiopaque calculi, and cystoscopy was performed with a cystolithotripsy. A large number of stones were removed, and analysis confirmed the composition was calcium oxalate (Figure 2).


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Volume : 19
Issue : 12
Pages : 1341 - 1344
DOI : 10.6002/ect.2021.0329

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From the Department of Nephrology, Jeddah Kidney Center, Kingdom of Saudi Arabia
Acknowledgements: The authors have not received any funding or grants in support of the presented research or for the preparation of this work and have no declarations of potential conflicts of interest.
Corresponding author: Faissal Shaheen, Department of Nephrology, Jeddah Kidney Center, Kingdom of Saudi Arabia