Hydration in chronic kidney disease

Hydration in chronic kidney disease

Summary

There is an important information gap in the Chronic Kidney Disease Management (CKD) Guidelines on the potential benefits of adequate hydration to prevent kidney damage. Although there is no conclusive evidence, experimental and population studies suggest that the amount of fluid ingested may be a risk factor for non-established CKD. The adverse renal effects of insufficient hydration may be mediated by increased vasopressin. In this sense, a generous water intake, at least to eliminate the osmotic load, may help to preserve renal function in patients with CKD who retain the capacity to generate high volume of urine.

The following theoretical analysis is intended to provide a reasonable argument for answering the question "How much should I drink ?: A standard diet generates approximately 650 mOsm of solutes, which must be excreted by the kidney. If we assume that the maximum urinary concentration is 1,200 mOsm / kg, at least 500 mL of urine will be necessary to eliminate the solute load. When there is advanced renal damage, the capacity of concentration is lost and isostenúrica urine is produced (250-300 mOsm / kg). If the required urinary volume is obtained by dividing the daily osmolar excretion by maximum urinary osmolality, diuresis of at least 2 L would be necessary to eliminate the usual solutes loading. This is achieved, depending on the extrarenal losses, with a liquid intake between 2.5 and 3.5 L per day.

Although the ability to generate high diuresis is maintained until advanced stages of CKD, this recommendation should be handled with maximum caution, and individualized. It is not applicable to patients with cardiorenal syndrome or with risk of hydrosaline retention. Likewise, forced ingestion may exceed the renal dilution capacity, and induce hyponatremia. Therefore, serum and urinary parameters should be monitored in order to prevent hyponatremia and dehydration, which is more frequent in summer and in elderly patients, who are the majority population in advanced CKD consultations.

Hydration and volume of urine
In our usual clinical practice, we must address both questions that concern patients, as well as verify adherence to our recommendations. The guidelines for the management of advanced chronic kidney disease (ERCA), we refer to the KDIGO as a special reference [1] , present important gaps in some of these issues. They are comprehensively analyzed in aspects such as proteinuria -predictor "star" in the progression of renal damage-, the controversial equations for calculating glomerular filtration (GF), the importance of blood pressure control, or the use of cardio and Renoprotectoras, among others. However, for optimal management of these patients we should evaluate other parameters such as urine volume, electrolytes, nitrogen ...

Frequently patients ask: Dr. How much should I drink ?, "because I urinate a lot, and if I drink more, I urinate more," is that bad? To these questions we must respond with convincing arguments. It is striking that the KDIGO Guidelines [1] do not set guidelines for water intake and desirable diuresis in the ERCA patient. Nor does the UPTODATE electronic treaty refer to diuresis, noting only the risk of hydrosaline retention in the complications section (http://www.uptodate.com/home: Overview of the management of chronic kidney disease in adults), especially if There is a history of congestive heart failure and systolic dysfunction. This is logical, but if we extend it to all patients, we can stay with the idea that we should restrict the liquids,

Despite this lack of information, in the literature we can find data on the benefits of adequate hydration to prevent kidney damage [2-4], and also another contradictory [5] . Recently, two excellent reviews have appeared [6] [7] of mechanisms by which low liquid intake can have adverse effects on the kidney and urinary tract in four disease scenarios: urolithiasis, urinary tract infections, bladder cancer and CKD . We will now deal with the potential effects of hydration on the progression of CKD.

Hydration and solutes loading in the healthy adult
The classic message of "at least 8 glasses of water per day" [8] is known , although there is only clear evidence of the benefits of forced hydration in nephrolithiasis [9] [10] .

The kidney needs water to filter and excrete waste products from the blood [9] [11] [12] . A standard diet represents approximately the generation of 650 mOsm * of solutes, which must be excreted by the kidney (13). This renal solute load (CRS) comes from ingested food and can be estimated from the following equation: CRS = Na + Cl + K + P + (N / 28). Na, K, Cl and P are expressed in mmol and N in mg. It is assumed that all proteins are converted to urea and all food minerals are eliminated by the kidney. From this formula, the urinary osm can be calculated as follows: Urine osm = CRS (mOsm / day) / (water intake - extrarenal water losses in L / day) [13] .

The healthy kidney is able to modify urinary osmolality (Osm) between 40-1,200 mOsm / kg of water approximately [12] [13] and the urinary volume will vary depending on the amount of osmoles that need to be excreted. Under normal circumstances, urine osm is two to three times higher than plasma, and diuresis is the mean daily in healthy individuals of 1.2-2.0 L [7] [14] . Likewise, the obligatory urinary volume, obtained by dividing the daily osmolar excretion (mOsm / day) by the maximum urinary osmolality (mOsm / kg H2O), will be approximately 500 mL of urine under conditions of maximum concentration.

This information can provide us with reasonable arguments to estimate the minimum diuresis necessary to eliminate solute loading in ERCA.

The amount of fluid ingested may be a non-established risk factor for CKD
Older renal physiology studies maintained that a high liquid intake could prevent kidney damage, even recommending diuresis of 3 L / day [15] . Subsequently, animal studies also found the benefits of high fluid intake in CKD [16] [17] , especially in adult polycystic disease (PQR).

More recently, Strippoli GF and col [4] performed two consecutive cross-sectional cuts in the general population over 50 years of age, showing that those individuals with higher liquid intake (higher quintile:> 3.2 L / day) had a lower risk of developing ERC. Also, Clark WF et al (3) analyzed the relationship between urine volume and renal impairment in a series of 2,148 individuals with GFR> 60 mL / min over a six-year follow-up period. The authors observed an inverse relationship between urine volume and renal damage; Emphasizing that those with a diuresis> 3 L showed less renal deterioration.

The work of Peraza S et al [18] , who studied a population exposed to insufficient and prolonged hydration, observed that these individuals suffered episodes of acute subclinical renal damage, and as a consequence, greater susceptibility to CKD. This manuscript and a lengthy review published in an accompanying editorial [19] warn us that the acknowledged "global warming" as a consequence of climate change may be an additional risk of CKD, especially in populations exposed to harsh working conditions in climates Warm

The possible association between renal damage and hydration in patients with CKD has been studied by Hebert et al. [5] using data from the MDRD study for the group with FG 25-55 mL / min / 1.73 m2 (20). The results were opposite to previous ones, ie to higher diuresis and lower urinary osm, more rapid progression of CKD in patients with and without PQR. These results have been questioned since the study was not designed for this objective, being more the consequence, than the cause of the rapid deterioration. It is also noteworthy that this observation was also made in patients with PQR, which is where the favorable effects of increased water intake are best observed.

The ADH is very much to blame
Data from the literature suggest that the adverse renal effects of insufficient hydration could be mediated by increased vasopressin or antidiuretic hormone (ADH) [2] [21] . ADH induces vasoconstriction of the efferent arteriole, glomerular hyperfiltration and renal flow redistribution; Increases tubular reabsorption of Na [22] and stimulates the synthesis of renin by activation of V2 receptors [23] . At the glomerular level a direct effect on mesangial proliferation has been described [24] . All of this results in a cascade of events that eventually produce tubulo-interstitial damage and nephrosclerosis [2] [12] [25] . Likewise, The reduction of endogenous ADH levels with high liquid intake leads to lower blood pressure, proteinuria, and potential benefit over renal function [25] [26] . In the PQR it is where the adverse effects of ADH have been better documented [2] [27] [28] [29] , showing that increased water intake slows the growth of cysts in animals via the direct suppression of The ADH  [2] [27] [28] [29] .

Dr. How much should I drink? Suggestions for clinical practice
We start from the premise that the previous information was obtained from population and experimental studies, and that there is no strong evidence to recommend forced hydration - but also not to restrict liquids - in CKD. That said, and waiting for more information, with the following theoretical analysis, we intend to provide a reasonable argument to answer the question that gives title to the editorial: Dr How much should I drink?

We said that to maintain homeostasis, the obligatory load of solutes to be excreted by the kidney is about 600 mOsm daily. We also know that when there is advanced renal damage, concentration capacity is lost and there is isosteric urine, between 250 and 300 mOsm / L on average [7] [14] , which we have verified in a series of patients at our visit Observing that these values ​​oscillate in a very narrow interquartile range (Table 1) . Therefore, in CKD with reduced active renal mass, more water must be excreted to remove solutes from the diet. Yes as we say before, The mandatory urinary volume is obtained by dividing the daily osmolar excretion (mOsm / day) by the maximum urinary osmolality (mOsm / kg H2O) [7] [14] , a diuretic of 2 L would be the minimum requirement to eliminate the usual solutes loading . This is achieved, depending on the extrarenal losses, with a liquid intake between 2.5 and 3.5 L per day. In general, we can estimate that 20% of the liquid intake comes from solids and 80% from water and other liquids [13] .

In this sense, the extended concept of "drink what you have thirst" may be insufficient, especially in elderly patients [30] and in summer seasons. The benefits of fluid intake beyond the demands of thirst, could be key to slow the progression of CKD [6] [7] . In fact, it is classic to see increases in serum creatinine in times of heat, or during episodes that occur with dehydration (fever, diarrhea, vomiting ...), and recover after adequate fluid intake. In view of these eventualities, we must also advise the patient for a reduction or temporary suspension of diuretics, renin-angiotensin-axis blockers or antihypertensives, as preventive measures for an acute and possibly irreversible deterioration,

On the other hand, we must be very cautious, the previous concepts are not applicable to patients with criteria of cardiorenal syndrome [31] . In the presence of precarious cardiac function (systolic dysfunction or even severe diastolic dysfunction), with a history of congestive heart failure, forced hydration carries the risk of hydrosaline retention and hyponatremia, especially when urinary Na + is low, indicating that compensatory neurohormonal mechanisms are Maximum stimulation.

In our ERCA consultation, in addition to periodically monitoring the urinary parameters, we have taken the routine of asking the patient to measure the diuresis of 24 hours. Once or twice a month, and thus compare with the volume they bring for periodic analysis. In this way we have the urinary volume of the patient in perspective, we increase the level of warning about this recommendation, and we also verify the so frequent: "Doctor the day I have to collect urine, I always urinate less." In (Table 1) (64 ± 14 years old, 78% male, 48% diabetic, 71% received loop diuretics), and urinary and urine urine urine urine output was measured in a series of 94 patients at our ERCA visit in stages 4 and 5 , Ie with a calculated GFR of less than 30 ml / min, And that unless explicit contraindication was given the recommendation to drink enough water to reach a urinary volume greater than 2 liters. Thus, we can verify that the high urinary volume is a characteristic of the CKD until very advanced stages (only 25% of the patients had diuresis inferior to 2 L). Likewise, the Osm shows that the urine is clearly isostenuric as it is classically described and urinary Na remains somewhat above the classic recommendations.

Serum Na values ​​have demonstrated the low risk of hyponatremia despite stimulating the liquid intake and reducing the Na of the diet. Only 4 patients had Na values ​​lower than 130 mEq / L without any symptoms. However, this warns us, that some patients also present a greater difficulty to dilute the urine, before a forced intake of liquids. Given that clinical practice is difficult to detect a priori, we must be aware of this eventuality that can pass clinically inadvertent, and that must be corrected early.