Salt matters

Last month I had the opportunity to review a paper, that in my mind, produces irrefutable evidence that restricting salt in your diet will slow the progress of the kidney cyst growth and therefore protect your kidneys for longer.  The authors themselves make the more modest claim that “moderate sodium restriction is beneficial to management of PKD” but after reading this study I have made major efforts to restrict my sodium intake.

The study was an additional analysis of some of the results from the HALT-PKD trial: Dietary salt restriction is beneficial to the management of autosomal dominant polycystic kidney disease Torres, Vicente E. et al.  Kidney International , Volume 91 , Issue 2 , 493 – 500

My original summary appears in the UK PKD charity newsletter.

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The image above shows how the kidneys are central to the maintenance of appropriate sodium levels in the body. Because of the way the kidneys work, sodium is initially filtered out into the nephron and then has to be reabsorbed. Most of this reabsorption occurs in the proximal tubules with the remaining adjustments made in the ascending Loop of Henle and the collecting ducts. It is easy to see therefore that the kidneys have to work pretty hard in this process and it is not a major leap to see why increasing the salt load on the kidney could effectively mean it wears out faster. Thats the simplistic view, it is obviously more complex than that and kidney function in PKD is far more complicated. The increasing cyst volume and thus decreasing amounts of normal healthy kidney tissue will certainly affect the way in which kidneys deal with sodium.

 

So, towards an understanding of this particular paper: 

What we know already:

It has long been recognised that people with ADPKD have raised blood pressure. Kidneys are central to regulating blood pressure (BP) and they do this through the Renin-Angiotensin-Aldosterone-System (RAAS) which involves a delicate balance of blood volume, renal blood flow, aldosterone and sodium (Na).

In the general population it is accepted that moderate salt (sodium) restriction has a beneficial effect on BP and cardiovascular events. But defining the optimum salt intake for people with chronic kidney disease has been controversial, with some studies producing unexpected results.

Reducing sodium intake has been shown to slow the progression of renal diseases where protein excretion in the urine (proteinuria) is common. However proteinuria is not a major feature of ADPKD, so would sodium restriction have the same effects?

The gold standard for assessing dietary sodium intake is to measure the sodium output, that is the urinary excretion of sodium (UNaE). This is more accurate than asking people to keep food diaries or extrapolating from single measurements of urine sodium content. The UNaE test entails a 24 hour urine collection. This was used in the CRISP study.

The CRISP study found that the UNaE was associated with the rate of total kidney volume (TKV) increase. This suggests that dietary intake of sodium may be related to the growth of the kidneys in PKD.

The HALT-PKD trial was to examine the effects of blood pressure control in PKD, and because it involved several hundred people with PKD it provides a valuable data resource for further analyses. This new paper uses the data from HALT-PKD to investigate whether sodium restriction slows the progress of the disease.

It has previously been shown that the increase in total kidney volume (TKV) can be used as a measure of progress of the disease, even in the early stages. In later stages the disease progress is measured by the fall in the glomerular filtration rate (eGFR).
Patients with ADPKD usually have sodium-sensitive hypertension.

 

What this paper adds:

The conclusion of the paper is that moderate sodium restriction in the diet could slow the progression of the disease.

It is worth looking a little closer at the paper to examine the validity of this claim and bearing in mind that the study was not specifically designed to examine sodium intake and disease progression.

The HALT-PKD study had two “arms” or groups of patients, one in early stages with good kidney function and the other of patients in later stages of the illness and moderately reduced kidney function. The current paper has analysed these two groups separately. Both groups demonstrated a relationship between urinary sodium output (UNaE) and progression of the disease. In group A, the early stages, the rate of increase in total kidney volume was associated with the averaged UNaE. In the group with less kidney function, the greater the urinary sodium excretion the larger the fall in kidney function, as measured by the estimated glomerular filtration rate (eGFR).

All of the patients involved in HALT-PKD were given advice on reducing their dietary sodium intake. Although long-term compliance with a low salt diet can be quite hard to achieve, the measurements of the urinary excretion of sodium did fall during the study showing that on the whole patients in the study did manage to keep to a sodium-restricted diet.

Because the original trial was assessing different degrees of blood pressure control it is important to note that the effect of salt restriction was noticed regardless of which BP treatment the patients were on.

The authors have added a single note of caution, that overzealous sodium restriction for patients on a ACE inhibitors for blood pressure medication could theoretically lead to some damage to the interstitial tissue (the tissue between the tubules) of the kidney. This has been shown is studies on rat models and is probably an unlikely situation given the modern diet.

For those interested, there are some complex statistical methods used in this study, with a purpose to ensure the effects seen were definitely related to the sodium intake and not some other variable.

This paper has clearly suggested a causal relationship between dietary sodium and increase in kidney size, irrespective of age, gender, race, BMI or BP treatment.

 

What does this mean for ADPKD?

A low salt diet in this instance was set as no more than 2.4g of sodium per day. This can also be stated as 100mEq per day – this measurement may be more commonly used in US.

If higher sodium intake is associated with faster decline in kidney function then it is clearly going to help if we take steps to reduce our sodium intake.

This is no easy task and we need both knowledge of the sodium content of foods and frequent reinforcement of the low sodium message in order to comply with this advice.

 

There is always a rider to any study, that individuals should only make dietary adjustments in consultation with their own medical advisors. But it is very likely that most of us would benefit from a low salt diet.

 

 

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