Am J Physiol Renal Physiol. Epub Feb Acid-base and endocrine effects of aldosterone and angiotensin II inhibition in metabolic acidosis in human patients. J Lab Clin Med. National Library of Medicine U. National Institutes of Health U. Department of Health and Human Services. The safety and scientific validity of this study is the responsibility of the study sponsor and investigators.
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You can also search for this author in PubMed Google Scholar. Interestingly, plasma potassium did not change significantly in the fruit and vegetable group all patients were on furosemide, and patients with serum potassium more than 4. These patients were divided into three groups of An oral bicarbonate supplementation group, fruit and vegetable group and standard treatment group.
All three groups received an angiotensin-converting enzyme ACE inhibitor with the goal to maintain a target systolic blood pressure of less than mmHg.
There are a few RCTs currently ongoing or actively recruiting, which may further shed light on the effectiveness of oral alkali therapy in preserving renal function, as well as other potential benefits such as an improvement in muscle strength and cardiac function[ 28 - 32 ]. The trial will look at the efficacy of oral sodum bicarbonate supplementation on physical performance, renal function, blood pressure, proteinuria and cost-effectiveness.
It will also cover a cohort of patients renal transplant recipients that have not formally been studied regarding chronic metabolic acidosis. CKD patients have a higher risk of fractures compared to the general population, largely due to a decrease in 1,25 hydroxylation of calcidiol OH-vitamin D and secondary hyperparathyroidism.
Bone is also used as a buffer for excess hydrogen ions in chronic metabolic acidosis, which leads to a loss of calcium and an exacerbation of bone fragility[ 33 ]. The preservation of bone health and the stabilisation of parathyroid hormone by the correction of metabolic acidosis has been demonstrated in a few studies[ 34 - 36 ].
Furthermore, a decrease in protein degradation is seen, at a biochemical level, with an increase in muscle mass and an improvement in physical function[ 7 , 37 - 39 ]. There has always been a concern regarding the worsening of hypertension, fluid overload and congestive heart failure CHF after the administration of oral sodium-based alkali supplementation in the CKD population due to sodium loading.
These potential theoretical adverse effects have not been proven in a clinical setting, although a majority of participants in the RCTs were excluded if uncontrolled hypertension or clinically overt CHF was present[ 7 , 25 ]. In one RCT, blood pressure was noted to be similar between the bicarbonate and standard care groups, with no CHF-related hospitalisation, and a similar increase in the use of diuretics and antihypertensive agents over the course of the study[ 7 ].
Goraya et al[ 27 ] reported a similar finding, with no significant difference in blood pressure between the standard care and bicarbonate-treated groups, and a similar requirement for enalapril. Two RCTs by Goraya et al[ 26 , 27 ] also demonstrated that a fruit and vegetable diet allowed better blood pressure control compared to both bicarbonate supplementation and standard care.
TRC , a novel sodium-free, non-absorbed hydrochloric acid binder, has shown efficacy in alleviating MA-CKD without effecting blood pressure, and may become widely available in the near future[ 40 ]. A plausible risk of increased vascular calcification exists once an acidotic environment has been resolved with oral alkali supplementation. However, there is currently a scarcity of studies to conclusively demonstrate this phenomenon[ 41 ].
A few RCTs demonstrated that a fruit and vegetable diet reduced the overall acid load and had a renoprotective effect[ 26 , 27 ]. Two interesting observations can be noted. Despite this, however, the urinary indices of renal injury were lower and GFR was preserved[ 26 ]. Even when oral alkali therapy was used in patients with CKD G2 and normal serum bicarbonate levels, a decline in the reduction of GFR was observed[ 20 ].
These findings correlate with the understanding that western, high animal meat diets are indirectly renotoxic due to their overall acid-inducing effect, and that alkaline agents, either fruits and vegetables or oral sodium bicarbonate, help to neutralize this excess acid[ 42 , 43 ]. It can be postulated that when fruits and vegetables associated with an alkaline effect are incorporated into a diet, they will be renoprotective at any CKD stage because of their ability to buffer acid.
Thus, the use of high potassium-containing fruits and vegetables in this category remains controversial[ 26 ]. Since none of the RCTs included uncontrolled hypertension and overt CHF patients, clinical judgment should be used when initiating oral alkali therapy in patients with an underlying history of CHF or hypertension requiring more than three agents to control[ 7 , 20 , 26 , 27 , 37 ].
The upper limit of serum bicarbonate levels once on oral alkali therapy is still speculative, with limited data available. In four of the RCTs, an average of 0. It is further suggested that dieticians in renal units get involved in designing a program for CKD G1-G3 regardless of serum bicarbonate that incorporates fruits and vegetables to reduce the overall acid load, and commence community programs to promote this.
A 1 mg dose of sodium bicarbonate approximately equates to 0. A mg sodium bicarbonate tablet contains 7. In a 70 kg patient, this is approximately 0.
Three additional tablets may have patient compliance issues, as sodium bicarbonate can lead to abdominal bloating. An unconventional approach is to utilise natural baking soda sodium bicarbonate , of which one teaspoon is equal to approximately mg of sodium bicarbonate. Thus, one-half of a teaspoon mixed in water should produce mg, which is equivalent to 31 mEq x 0. The cost per mg of sodium bicarbonate tablets including enteric-coated tablets is approximately 0.
If used at 0. MA-CKD is a complication that is often overlooked in clinical practice. Current evidence suggests that it contributes to renal function decline, and that appropriate management would lead to better CKD outcomes in terms of renal function preservation, muscle function, bone health and economic burden. Oral alkali therapy has the potential, when combined with other known interventions like blood pressure control and glycaemic control, to prolong the time before reaching end-stage renal disease.
The recommendations offered here can be used as a basis to develop more detailed guidelines in the Republic of Ireland and around the world. Larger ongoing RCTs highlighted in this review will perhaps provide more conclusive evidence. Manuscript source: Unsolicited manuscript. Specialty type: Urology and Nephrology. Country of origin: Ireland.
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