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Letters to the Editor

Fluid Intake Postrenal Transplant; Drink to Thirst or Drink to Target

Does It Matter?

Mao, Catherine1; Chacko, Bobby FRACP1,2

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doi: 10.1097/TP.0000000000003027
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A recent case in our unit of a 40-year-old who presented 5 years postrenal transplant with 2 episodes of hyponatremia (sodium 122 mmol/L) induced seizures, contributed by excessive water intake (~ 4 L/d) prompted us to highlight this issue.

Renal transplant recipients are repeatedly advised to maintain a generous fluid intake. So much so that it is not uncommon to see these patients carrying water bottles to keep themselves hydrated. Everyone can feel like they are conveying deep truths by suggesting you need to drink more water.

High fluid intake (HFI) in excess of 3 L/day is commonly recommended. Despite being usual practice, the evidence for this is surprisingly limited. Polyuria immediately after a renal transplant is not unusual and is often exaggerated by the need and tendency to maintain a positive fluid balance postoperatively. The assumption that suboptimal function of the posttransplant proximal tubule, associated with a concentration defect, can lead to dehydration may have influenced this practice. While this may be true in the immediate postrenal transplant period, recommendations mandating HFI subsequently may be incorrect.

Evidence for a beneficial effect of a HFI in chronic kidney disease (CKD) is based primarily in rats, where increasing fluid intake suppressed maladaptive renal hypertrophy and interstitial fibrosis.1 However, in the CKD Water Intake Trial clinical trial among adults with stage 3 CKD, drinking more water (compared with usual fluid intake alone) did not significantly slow the decline in kidney function after 1 year.2

The 3 studies (Table 1) that examined the relationship between fluid intake and graft function in renal transplant recipients demonstrated no significant effect of HFI on graft survival and function, suggesting no apparent benefit to this practice.

TABLE 1
TABLE 1:
Comparison of studies on fluid intake and posttransplant renal function

If HFI does not have measurable effect in the posttransplant population, the next natural question is what advice, if any, is warranted instead? The thirst mechanism is a well-regulated body system that works predictably. It is possible that drinking to thirst is an adequate alternative for graft survival. In fact, drinking to thirst is increasingly advised in sporting competition over programmed drinking as it is found to be sufficient to prevent both dehydration and exercise-associated hyponatremia. However, there is limited available research of the extent to which these physiological mechanisms can compensate for changed conditions such as in renal transplant or CKD.

In a qualitative study of self-care strategies in 82 renal transplant recipients, 38% reported “not being thirsty” as a barrier to postoperative fluid intake.6 These patients also reported difficulty in drinking fluids ad libitum due to ingrained fluid restriction behaviors while on dialysis. For most patients, this transition resolved over several weeks; however, it also affirms the need for patient-centered advice and support. Given the unique barriers that renal transplant recipients face both behaviorally and possibly physiologically, drinking to thirst is not an adequate guide for fluid intake without further evidence at this stage.

While there is no debate about the dangers of fluid depletion, the widespread recommendation for HFI of > 3 L/day in the posttransplant period is not evidence based and may be harmful as in our case. Ideally, a well-designed randomized control study with a sufficiently large sample size and adequate control of variables including time since transplant, living versus deceased donors, and reliably measured fluid intake, would be able to further define this relationship and inform clinical practice.

Until then, recommendations whether to drink to target or drink to thirst should be patient centered to avoid both underhydration and overhydration. Renal transplant recipients need to know….too little water is harmful and so is too much water!

REFERENCES

1. Sugiura T, Yamauchi A, Kitamura H, et al. High water intake ameliorates tubulointerstitial injury in rats with subtotal nephrectomy: possible role of TGF-beta.Kidney Int1999551800–1810
2. Clark WF, Sontrop JM, Huang SH, et al. Effect of coaching to increase water intake on kidney function decline in adults with chronic kidney disease: the CKD WIT randomized clinical trial.Jama20183191870–1879
3. Gordon EJ, Prohaska TR, Gallant MP, et al. Longitudinal analysis of physical activity, fluid intake, and graft function among kidney transplant recipients.Transpl Int200922990–998
4. Magpantay L, Ziai F, Oberbauer R, et al. The effect of fluid intake on chronic kidney transplant failure: a pilot study.J Ren Nutr201121499–505
5. Weber M, Berglund D, Reule S, et al. Daily fluid intake and outcomes in kidney recipients: post hoc analysis from the randomized ABCAN trial.Clin Transplant201529261–267
6. Gordon EJ, Prohaska TR, Gallant M, et al. Self-care strategies and barriers among kidney transplant recipients: a qualitative study.Chronic Illn2009575–91
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