The restriction of Na is an unequivocal recommendation to control of hypertension and volume retention.19 Clinical guidelines1,3 recommend an intake of Na <2g/day, which corresponds to 5g of salt, unless there is a specific contraindication. However, there is no mention of the importance of monitoring the adherence to this prescription and how to do it.

Urinary Na determination is the easiest way to monitor saline intake.20–24 Ancient work has verified that Na is absorbed quickly and effectively in the intestinal mucosa (a 98%), therefore, in a situation of homeostasis urine Na is a good indicator of the intake.21,22 It is postulated that the use of diuretics can be a limitation for the value of natriuresis. However, in a patient on balance, the urinary Na reasonably reflects saline intake.

The Na intake is calculate using a simple equation: Na in mEq/urine 24h×0.058=daily salt intake (g).

In the “real world” the usual intake of salt in the population is 9–12cg/day, and even higher in many regions, which corresponds to a urinary elimination of Na of 160–200mEq./day or even more.25 Achieving a saline intake of 5–6g per day (80–100mEq of Na/day), is possible, but very difficult to achieve even in adherent patients.

Table 2 shows examples of the correspondence between saline intake and urinary Na, and it should be emphasized the importance of measuring Na in 24-h urine to optimize patient management and adherence to our recommendations.

The benefits of dietary protein restriction in CKD are reasonably accepted. The aim is to delay CKD progression of – especially if proteinuria is present – but there are also beneficial in other nutritional aspects.26–31 This concept would not be applicable to patients with polycystic kidney disease, very doubtful in non-proteinuric nephropathies, but especially beneficial in diabetic nephropathy. With the progression of renal damage, nitrogen products accumulate proportionally to the loss of renal function. In fact, protein restriction has prevailed for decades and has been the cornerstone of treatment when dialysis did not exist.

Collecting information from previous studies,32 the KDIGO Guidelines recommend a protein intake of 0.8g/kg/day in adults with GFR<30ml/min/1.73m2, this is being assumed in most guidelines and consensus documents.33 Based on our experience, we consider that achieving a protein restriction of 0.8–0.9g/kg/day is a reasonable objective that is possible to achieve.

Now, returning the ACKD scenario, we would like to point out the importance of knowing the patient's protein intake and adherence to our recommendations. It has been verified that the determination of urinary urea nitrogen (UUN) is a useful parameter to estimate protein intake. The classic equation described by Maroni et al.34 is useful to evaluate the protein intake in patients in metabolic equilibrium. The protein intake is derived from the estimation of UUN, adjusting for weight and proteinuria: UUN (g)+0.031×weight (kg)+proteinuria (g). This result multiplied by 6.25 gives us approximate information on protein intake. This formula has been reasonably verified by other authors,35 and even with its limitations we consider that it should be mentioned in the clinical practice guidelines. In Table 3, based on unpublished results of our ACKD outpatient clinic, we show the approximate relationship between the values of UUN and protein intake, where we observe that the median of NUU (7.8g) corresponds to a protein intake of 49–55g depending on the weight used in the equation.

The evaluation of the acid load and urinary potassium (K) are not frequently used in clinical practice. However, recent data emphasize the importance of controlling the acid load of the diet as a modifiable risk factor for the progression of kidney disease.36

The endogenous production of acids derives mainly from the intake of proteins and phosphate. The production of alkali comes from organic anions such as citrate and acetate, naturally bound to cations such as K which are found primarily in vegetables and fruits. The difference between the two results in the acid load, which is normally eliminated by the kidneys as ammonium and titratable acid, and in a standard diet is approximately 1mEq/kg/day.

Scialla et al.37 described a direct association between dietary acid load and renal deterioration. In CKD, with the reduction of nephron mass, each of the remaining nephron increases the ammoniogenesis and distal excretion of acid mediated by RAAS and endothelin-1, which results in kidney damage.36,38,39 In fact, the KDIGO Guidelines recommend giving oral bicarbonate supplements in case the serum concentration is less than 22mmol/l.

Based on these premises, it is postulated that the reduction of the acid load may be an additional strategy in the nutritional management of this population. The acid load is determined by the balance of the foods that induce acid (meats, eggs, dairy products, cereals) and those that induce alkali (fruits and vegetables). A greater intake of the latter may contribute to a reduction of the acid load without the need for excessive protein restriction and bicarbonate intake.36,37,40–42 A prudent intake of foods rich in K, may contribute to achieve a healthier diet in this population. This subject has been recently reviewed by Kalantar-Zadeh et al.43

Obviously, in ACKD the risk of hyperkalemia is an important limitation. Currently there are no clinical studies that guarantee the safety of a more free diet in vegetables and fruits in this population. However, in well-nourished patients, with good urinary output and in a non-catabolic state, their judicious intake of fruits and vegetables avoiding prolonged fasting44–46 (an important and frequently forgotten recommendation), may be a measure both nutritionally healthy and renoprotective (37, 47–49). Obviously, diabetic patients or those treated with beta-blockers and/or RAAS blockers will be subject to greater vigilance, especially those who receive K-sparing diuretics.50

The acid load may be estimated indirectly from the intake of nutrients or from the urinary elimination of ions, for which various equations have been postulated36,37,47,48,51; perhaps the simplest is the following:

Acid load (mEquiv./day): −10.2+54.5×(protein intake [g/day]/K intake [mEq/day]).36,37,48

The protein and K intake may be obtained from the elimination of UUN and K (1mEquiv. of K⇔39mg), which, with all its limitations, are considered indirect indicators of protein intake and alkaline load, respectively.37,41,52 Whereas the determination of the UUN to assess protein intake is well established,34,35 the value of the urinary K as indicator of the alkaline load is not that well recognized.

On a standard diet, the range of urinary elimination of K is wide, 50–200mEq/day, which is equivalent to 2000–7800mg/day. In hemodialysis patients the adverse effect of K retention is well known. Kalantar-Zadeh et al.53 suggest that the K intake should be <3g/day; the authors also emphasizes the importance of a healthy diet, with prudent intake of fruit and vegetable, without proposing specific amounts.43

Several authors have explored the impact of acid loading, both in population studies37 and in ACKD patients, even using a diet relatively free on fruits and vegetables.51 The latter described a decrease in the acid load, with a urinary elimination of K of 69.9±12.39mE/day, equivalent to an average of 2800mg/day, without relevant change in serum K concentration (4. 1±0.1mEq/l).

Since the limits in this recommendation have not been established, we propose a prudent intake of vegetables and fruits, around 2800–3000mg of K/day (see http://www.revistanefrologia.com/es-monoografias-nefrologia-dia-articulo-manejo-nutricional-enfermedad-renal-cronica-99), trying to maintain urinary K levels below 70–75mEq/day.37,43,47–49,51,54 The key concepts are presented in Table 4.

In the normal adult, the calcium (Ca) balance is relatively neutral when the intake is between 750 and 1740mg/day.55 In this context, the urinary excretion of Ca ranges between 200 and 300mg/day, thus there is variable intestinal absorption from 20 to 60%, depending to a large extent on the amount of circulating levels of 1,25(OH)2D3.

In ACKD, urinary excretion of Ca is much lower, in a range of 20–60mg/day,56–58 although fractional excretion (percentage of filtered Ca that is eliminated in the urine) is slightly elevated (1.1–1.4%, normal <1%). Hill et al.,56 in an interesting study in patients with CKD stages 3–4, described an intestinal absorption of Ca truthfully low, around 17–22%, and urinary Ca excretion of 40–42mg/day.

In ACKD, calciuria is not a parameter that provides relevant information in clinical practice, but it is useful in the experimental setting, especially in studies that involve the balance of Ca and the use of drugs such as calciomimetics, vitamin D analogs or phosphate binders (P).

The next difficulty in estimating the P balance is intestinal absorption. The net absorption is very variable, between 40% and 80%. Therefore, for an intake between 800 and 1600mg/day, the absorption may vary from 320 to 1280mg, being somewhat lower in ACKD and in hemodialysis.64–67

In this sense, the values of urinary P (Pur), along with those of UUN may provide relevant information, since the Pur must reliably reflect the amount P absorbed, not the ingested amount. If we accept that the absorption is of 60–70%, this parameter can be useful to advise the patient in his diet and monitor his adherence.

Morimoto et al.61 found in the general population a close relationship between the P and protein intake obtained from the dietary survey and the urinary parameters of P and UUN, respectively (Fig. 2). The latter were derived from the following equation: intake of P=Pur×0.65 (assumes that the intestinal absorption is 65%) and protein intake is calculated from the UUN using the Maroni equation.34 Despite the biases described by the authors (inaccuracy of the dietary record and variable intestinal absorption of P) this analysis highlights the information that can be extracted from the determination of the Pur and UUN.

Fig. 2.

Association between intake of protein and phosphorus, assessed by dietary record (RD) and urinary collection (UC).

(0.15MB).

Taken from Morimoto et al.61

In ACKD it has been possible to verify the close association between the UUN and the Pur. The data published by Caravaca et al.68 can be superimposed to those obtained in our population, as illustrated in Fig. 3. If we assume that the intestinal absorption of P was 60–70%, we can indirectly estimate that the actual intake of P was within a range of 650–900mg. These data are very consistent with those obtained from dietary surveys (Fig. 1) in hemodialysis patients. Slightly higher values were published in CKD E3 patients,69 where a mean Pur of 792mg was collected (95% CI: 646–938).

Fig. 3.

Correlation between urinary excretion of phosphorus and urinary urea nitrogen in patients with advanced chronic kidney disease. The slopes of the 2 series are totally superimposable.

(0.12MB).

The information provided by the ratio P/protein in urine described by Caravaca et al.68 is very interesting; it is provides values of 8.22±2.34mg of P/g protein. These values are lower than those published from the dietary registry59 that presented the P ingested, not the absorbed.

Finally, Caravaca et al.68 conducted a novel and very interesting analysis based on the corrected Pur for glomerular filtration rate (GFR). A Pur of 35–40mg for each ml/min of GFR marked the limit for the development of hyperphosphataemia (serum P>4.5mg/dl). That is to say, for patients with GFR<25ml/min phosphaturia should be less than 800mg.

The combined analysis of these data suggests that for patients with GFR<25ml/min, and prescribing a diet of 0.8–0.9g/kg/day of protein, a reasonable target is a urinary P less than 800mg/day, and with GFR<15ml/min, urinary P excretion should be less than 600mg.

It is still pending to quantify the impact of inorganic P contributed by additives and soft drinks, being also the Pur and the urinary quotient P/UUN the parameter that could best identify those patients who abuse these products.

The fractional excretion (FEP=Pur×Serum Cr/Serum P×Urine Cr) and its complementary parameter, the tubular reabsorption of P (TRP [%]=1−FEP) also provides relevant information. With the progressive loss of functioning renal mass the TRP is reduced and it increases the FEP, with an increase of FGF23 and PTH. In our population with CKD stage 4 and 5 we observe an average TRP of 59% (corresponding to FEP of 41%), which suggests P retention, despite documenting normal serum levels of P. In the study by González Parra et al.,69 performed in patients with CKD stage 3, it was observed a TRP of 66–74%. Thus TRP emerges as an valuable marker of abnormal mineral metabolism in CKD.67,70

Urinary creatinine concentration is an essential parameter in renal patients. It is used to calculate creatinine clearance and the albumin/creatinine ratio in morning urine samples. In general, urinary excretion of creatinine in the normal adult is very variable ranging from 500 to 2000mg/day, depending largely on age and muscle mass. A practical way to express the normal range of urine creatinine excretion is as follows: male 14–26mg/kg/day, female 11–20mg/kg/day. Urinary creatinine values within this range suggests that 24h urine collection has been adequate.71

In ACKD, the ability to generate a high volume of urine is preserved until more advanced stages of CKD.

The amount of liquid ingested may be a risk factor for CKD that is not established.

Achieving an adequate and individualized high urinary flow may help to preserve kidney function.

Controlling the diuresis of 24h is a necessary parameter to prevent the undesired effects of inadequate hydration (Table 1).

The restriction of Na is a primary recommendation for Blood Pressure control and prevention of hydrosaline retention.

The urinary Na is a useful and affordable determination to monitor saline intake (Table 2).

Protein restriction is considered a first step to protect renal function in ACKD.

The determination of UUN has been verified as a useful parameter to estimate the protein intake (Table 3).

The reduction of the acid load can be a complementary nutritional strategy in the management of CKD patients.

The acid load can be estimated indirectly from the dietary survey or by measuring the urinary excretion of UUN and K.

A more liberal diet of vegetables and fruits (avoiding prolonged fasting), along with protein restriction, may be nutritionally healthy and renoprotective.

There is a close correlation between intake of protein and P.

The combined analysis of both may help to minimize the P load, without inadequately low protein restriction.

This correlation has been verified from the urinary parameters of UUN and P, which reflect the P absorption versus intake.

Monitoring phosphaturia and UUN may help to assess the intake of P in the form of additives and soft drinks.