Low dietary K levels have been associated with increasing renal Ca excretion in humans, indicating a higher risk of calcium oxalate (CaOx) urolith formation. Therefore, the present study aimed to investigate whether dietary K also affects the urine composition of cats. A total of eight adult cats were fed diets containing 0·31 % native K and 0·50, 0·75 and 1·00 % K from KCl or KHCO3 and were evaluated for the effects of dietary K. High dietary K levels were found to elevate urinary K concentrations (P< 0·001). Renal Ca excretion was higher in cats fed the KCl diets than in those fed the KHCO3 diets (P= 0·026), while urinary oxalate concentrations were generally lower in cats fed the KCl diets and only dependent on dietary K levels in cats fed the KHCO3 diets (P< 0·05). Fasting urine pH increased with higher dietary K levels (P= 0·022), reaching values of 6·38 (1·00 % KCl) and 7·65 (1·00 % KHCO3). K retention was markedly negative after feeding the cats with the basal diet ( − 197 mg/d) and the 0·50 % KCl diet ( − 131 mg/d), while the cats tended to maintain their balance on being fed the highest-KCl diet ( − 23·3 mg/d). In contrast, K from KHCO3 was more efficiently retained (P= 0·018), with K retention being between − 82·5 and 52·5 mg/d. In conclusion, the dietary inclusion of KHCO3 instead of KCl as K source could be beneficial for the prevention of CaOx urolith formation in cats, since there is an association between a lower renal Ca excretion and a generally higher urine pH. The utilisation of K is distinctly influenced by the K salt, which may be especially practically relevant when using diets with low K levels.

Identifying dietary modifications that potentiate the blood pressure (BP)-lowering effects of antihypertensive medications and that are practical for free-living people may assist in achieving BP reduction goals. We assessed whether two dietary patterns were effective in lowering BP in persons on antihypertensive therapy and in those not on therapy. Ninety-four participants (38/56 females/males), aged 55·6 (sd 9·9) years, consumed two 4-week dietary regimens in random order (Dietary Approaches to Stop Hypertension (DASH)-type diet and low-Na high-K (LNAHK) diet) with a control diet before each phase. Seated home BP was measured daily for the last 2 weeks in each phase. Participants were grouped based on antihypertensive drug therapy. The LNAHK diet produced a greater fall in systolic BP (SBP) in those on antihypertensive therapy ( − 6·2 (sd 6·0) mmHg) than in those not on antihypertensive therapy ( − 2·8 (sd 4·0) mmHg) (P = 0·036), and this was greatest for those on renin–angiotensin system (RAS) blocker therapy ( − 9·5 (sd 6·4) mmHg) (interaction P = 0·007). The fall in SBP on the DASH-type diet, in those on therapy (overall − 1·1 (sd 6·2) mmHg; renin–angiotensin blocker therapy − 4·2 (sd 4·7) mmHg), was not as marked as that observed on the LNAHK diet. Dietary modifications are an important part of all hypertension management regimens, and a low-Na and high-K diet enhances the BP-lowering effect of antihypertensive medications, particularly those targeting the RAS.