Hyperchloremic metabolic acidosis after plasma exchange in a patient with renal transplant rejection: A case report.

Therapeutic plasma exchange (TPE) is an effective treatment for several renal disorders, including renal transplant rejection. However, repeated plasma exchanges can result in various metabolic disturbances and complications. We present a 61-year old male with a medical history of type 2 diabetes, hypertension, successfully treated multiple myeloma, and a post-mortem kidney transplantation 7 months prior to presentation. The patient was hospitalized with an antibody-mediated transplant rejection for which treatment with methylprednisolone, TPE with a 40 g/L albumin solution as a replacement fluid, and intravenous immunoglobulins was initiated. After four TPE treatments, the patient developed gastrointestinal complaints and muscle weakness. Despite daily oral bicarbonate supplementation, laboratory tests revealed a hyperchloremic metabolic acidosis: bicarbonate 11.7 mmol/L, chloride 111 mmol/L, and sodium 138 mmol/L. Metabolic acidosis due to citrate accumulation was ruled out with a normal total-to-ionized calcium ratio. After treatment with intravenous bicarbonate supplementation, the symptoms disappeared. Analysis of the albumin solution showed a chloride concentration of 132 mmol/L. This is the first case that describes severe metabolic acidosis after multiple sessions of TPE with an albumin solution in a patient with impaired renal function. The hyperchloremic metabolic acidosis is the result of administration of large volumes of an albumin solution with high chloride concentrations. Special attention should be paid to the acid-base balance during TPE in patients with impaired renal function. Future research should investigate the incidence of hyperchloremic metabolic acidosis during TPE in patients with impaired renal function.

Alcoholic Ketoacidosis: Etiologies, Evaluation, and Management.

BACKGROUND: Alcoholic ketoacidosis (AKA) is defined by metabolic acidosis and ketosis in a patient with alcohol use. This is a common presentation in the emergency department (ED) and requires targeted therapies. OBJECTIVE: This narrative review evaluates the pathogenesis, diagnosis, and management of AKA for emergency clinicians. DISCUSSION: AKA is frequently evaluated and managed in the ED. The underlying pathophysiology is related to poor glycogen stores and elevated nicotinamide adenine dinucleotide and hydrogen. This results in metabolic acidosis with elevated beta-hydroxybutyrate levels. Patients with AKA most commonly present with a history of alcohol use (acute or chronic), poor oral intake, gastrointestinal symptoms, and ketoacidosis on laboratory assessment. Patients are generally dehydrated, and serum glucose can be low, normal, or mildly elevated. An anion gap metabolic acidosis with ketosis and electrolyte abnormalities are usually present on laboratory evaluation. Management includes fluid resuscitation, glucose and vitamin supplementation, electrolyte repletion, and evaluation for other conditions. CONCLUSIONS: Emergency clinician knowledge of the evaluation and management of AKA is essential in caring for these patients.

[Starvation ketoacidosis during prolonged fasting of 26 days]. / Hypercétose dans un contexte de jeûne prolongé de 26 jours.

Ketosis is a metabolic situation involving an increase in blood and urine concentrations of ketones that, when prolonged, leads to acidosis. Moderate ketosis usually appears after a fast of a few hours, but its prolongation exposes to hyperketosis. Observation: A 25-year-old woman presented to the emergency department for cohercitive vomiting. She was fasting for a long time in a spiritual setting and had a restricted diet limited to water and vitamin supplements. Clinical and biological assessment was in favour of fasting ketoacidosis. Evolution was favorable with intravenous hydration, poly-ionic and micronutrient supplementation and a gradual resumption of oral feeding. Conclusion: We report the case of a patient with fasting ketoacidosis. Besides consequences of this ketoacidosis, the challenge was also in resuming oral feeding in order to avoid a potentially fatal inappropriate renutrition syndrome.

A complicated chinese herbal medicine nephrotoxicity.

Chinese herbal medicine is widely used globally. In many instances, it is associated with severe adverse outcomes. We report case of a Chinese herbal nephropathy occurring in a 43-year-old woman showing renal impairment, metabolic acidosis, Stokes - Adams syndrome, hypernatremia, and hypokalemia, characteristics not usually encountered in published cases.

Intralipid and haemodialysis in caffeine overdose.

A 26-year-old woman presented after an intentional ingestion of 20 g of caffeine. She suffered a profound respiratory alkalosis with metabolic acidosis, hypokalaemia and sustained polymorphic ventricular tachycardia. She was treated with intravenous intralipid and haemodialysis, and her arrhythmia was controlled using magnesium sulphate. Once invasively ventilated and unable to hyperventilate the patient became acidotic and required intravenous bicarbonate to correct her acid-base status. Two days following the overdose the patient was extubated, haemodialysis was stopped and norepinephrine was weaned off. The patient was discharged after a further 7 days. Serial caffeine levels were taken during this patient's care; the highest measured caffeine concentration 7 hours after ingestion was 147.1 mg/L. The known lethal dose of caffeine is 80 mg/L. Intralipid and haemodialysis represent a new and viable treatment in life-threatening caffeine overdose. Intravenous magnesium may terminate unstable arrhythmias in caffeine-poisoned patients.

Severe clinical manifestation of mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase deficiency associated with two novel mutations: a case report.

BACKGROUND: Mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase (mHS) deficiency is an autosomal recessive inborn error of metabolism, which will give rise to failure of ketogenesis in liver during illness or fasting. It is a very rare disease with only a few patients reported worldwide, most of which had a good prognosis after proper therapies. CASE PRESENTATION: We report a 9-month-old boy with mHS deficiency presenting with unusually severe and persistent acidosis after diarrhea and reduced oral food intake. The metabolic acidosis persisted even after supplementation with sugar and alkaline solution. Blood purification and assisted respiration alleviated symptoms, but a second onset induced by respiratory infection several days later led to multiple organ failure and death. Urine organic acid analysis during the acute episode revealed a complex pattern of ketogenic dicarboxylic and 3-hydroxydicarboxylic aciduria with prominent elevation of glutaric acid and adipic acid, which seem to be specific to mHS deficiency. Plasma acylcarnitine analysis revealed elevated 3-hydroxybutyrylcarnitine and acetylcarnitine. This is the first report of elevated 3-hydroxybutyrylcarnitine in mHS deficiency. Whole exome sequencing revealed a novel compound heterozygous mutation in HMGCS2 (c.100C > T and c.1465delA). CONCLUSION: This severe case suggests the need for patients with mHS deficiency to avoid recurrent illness because it can induce severe metabolic crisis, possibly leading to death. Such patients may also require special treatment, such as blood purification. Urine organic acid profile during the acute episode may give a hint to the disease.

Zero balance ultrafiltration using dialysate during nationwide bicarbonate shortage: a retrospective analysis.

BACKGROUND: Zero balance ultrafiltration (Z-BUF) utilizing injectable 8.4% sodium bicarbonate is utilized to treat hyperkalemia and metabolic acidosis associated with cardiopulmonary bypass (CPB). The nationwide shortage of injectable 8.4% sodium bicarbonate in 2017 created a predicament for the care of cardiac surgery patients. Given the uncertainty of availability of sodium bicarbonate solutions, our center pro-actively sought a solution to the sodium bicarbonate shortage by performing Z-BUF with dialysate (Z-BUF-D) replacement fluid for patients undergoing cardiopulmonary bypass. METHODS: Single-center, retrospective observational evaluation of the first 46 patients at an academic medical center who underwent Z-BUF using dialysate over a period of 150 days with comparison of these findings to a historical group of 39 patients who underwent Z-BUF with sodium chloride (Z-BUF-S) over the preceding 150 days. The primary outcome was the change in whole blood potassium levels pre- and post-Z-BUF-D. Secondary outcomes included changes in pre- and post-Z-BUF-D serum bicarbonate levels and the amount of serum bicarbonate used in each Z-BUF cohort (Z-BUF-D and Z-BUF-S). RESULTS: Z-BUF-D and Z-BUF-S both significantly reduced potassium levels during CPB. However, Z-BUF-D resulted in a significantly decreased need for supplemental 8.4% sodium bicarbonate administration during CPB (52 mEq ± 48 vs. 159 mEq ± 85, P < 0.01). There were no complications directly attributed to the Z-BUF procedure. CONCLUSION: Z-BUF with dialysate appears to be analternative to Z-BUF with sodium chloride with marked lower utilization of intravenous sodium bicarbonate.

Fruit and Vegetable Treatment of Chronic Kidney Disease-Related Metabolic Acidosis Reduces Cardiovascular Risk Better than Sodium Bicarbonate.

BACKGROUND: Current guidelines recommend treatment of metabolic acidosis in chronic kidney disease (CKD) with sodium-based alkali. We tested the hypothesis that treatment with base-producing fruits and vegetables (F + V) better improves cardiovascular disease (CVD) risk indicators than oral sodium bicarbonate (NaHCO3). METHODS: We randomized 108 macroalbuminuric, matched, nondiabetic CKD patients with metabolic acidosis to F + V (n = 36) in amounts to reduce dietary acid by half, oral NaHCO3 (HCO3, n = 36) 0.3 mEq/kg bw/day, or to Usual Care (UC, n = 36) to assess the 5-year effect of these interventions on estimated glomerular filtration rate (eGFR) course as the primary analysis and on indicators of CVD risk as the secondary analysis. RESULTS: Five-year plasma total CO2 was higher in HCO3 and F + V than UC but was not different between HCO3 and F + V (difference p value < 0.01). Five-year net eGFR decrease was less in HCO3 (mean -12.3, 95% CI -12.9 to -11.7 mL/min/1.73 m2) and F + V (-10.0, 95% CI -10.6 to -9.4 mL/min/1.73 m2) than UC (-18.8, 95% CI -19.5 to -18.2 mL/min/1.73 m2; p value < 0.01) but was not different between HCO3 and F + V. Five-year systolic blood pressure was lower in F + V than UC and HCO3 (p value < 0.01). Despite similar baseline values, F + V had lower low-density lipoprotein, Lp(a), and higher serum vitamin K1 (low serum K1 is associated with coronary artery calcification) than HCO3 and UC at 5 years. CONCLUSION: Metabolic acidosis improvement and eGFR preservation were comparable in CKD patients treated with F + V or oral NaHCO3 but F + V better improved CVD risk indicators, making it a potentially better treatment option for reducing CVD risk.

Cleistanthus collinus poisoning: a case report of intentional poisoning.

We report a case of 50-year-old male patient from tribal area in South Indian state of Telangana, who ingested the liquid extract from crushed leaves of the plant, cleistanthus collinius with the intention of self-harm. Immediate gastric lavage and activated charcoal administration was done and the patient was subsequently admitted into an acute medical care unit. During first 24 hours of monitoring, the patient was clinically stable. There was mild normal anion gap metabolic acidosis and hypokalaemia on arterial blood gas (ABG) and was corrected accordingly. On second day of admission he developed acute onset shortness of breath. Chest auscultation revealed extensive bilateral coarse crackles. Chest X-ray was suggestive of acute respiratory distress syndrome (ARDS). The patient had to be intubated. Continuous renal replacement therapy (CRRT) was initiated in view of worsening metabolic acidosis and unstable haemodynamics. In spite of appropriate intensive care measures, the patient succumbed to illness. Immediate gastric lavage and activated charcoal administration was done and the patient was subsequently admitted into an acute medical care unit. During first 24 hours of monitoring, the patient was clinically stable. There was mild normal anion gap metabolic acidosis and hypokalaemia on ABG and was corrected accordingly. On second day of admission, he developed acute onset shortness of breath. Chest auscultation revealed extensive bilateral coarse crackles. Chest X-ray was suggestive of ARDS. The patient had to be intubated on day 2. CRRT was initiated in view of worsening metabolic acidosis and unstable haemodynamics. In spite of appropriate intensive care measures, the patient gradually deteriorated, had cardiac arrest and passed away on day 5 of his hospital stay.

Alpha lipoic acid intoxication: An adult.

INTRODUCTION: Alpha lipoic acid (ALA) is a potent antioxidant used to treat a variety of disorders. Although ALA is considered a very safe supplement and intoxication is very rare, acute high-dose ingestions can cause mortality. In this report, we discuss a very rare case of ALA intoxication to increase awareness of this issue. CASE REPORT: A 22-year-old female was referred to our emergency department with ALA intoxication after ingesting a total of 18g of ALA with a suicidal intention. The patient was found in an altered mental state and confused. During the physical examination, the patient's Glasgow Coma Scale was 13 (E4M6V3); however, she was neither alert nor oriented. Vital signs revealed a mildly decreased blood pressure, tachycardia, and an increased respiratory rate. Cranial nerve examination was normal except a horizontal gaze nystagmus. Laboratory testing showed a decompensated metabolic acidosis. T wave inversions were seen in the electrocardiography (EKG). The patient was treated with supportive treatment and discharged within three days of intensive care unit (ICU) admission. CONCLUSION: ALA is a very common supplement that is easily accessible worldwide. Although ALA intoxication is very rare, it is sometimes seen after accidental or suicidal acute ingestion. Neurologic effects, metabolic acidosis, and t wave inversions in the EKG are observed when this acute poisoning occurs. Supportive treatment should be the main therapy.

Peptide Receptor Radionuclide Therapy-Induced Gitelman-like Syndrome.

Peptide receptor radionuclide therapy (PRRT) is a molecular-targeted therapy in which a somatostatin analogue (a small peptide) is coupled with a radioligand so that the radiation dose is selectively administered to somatostatin receptor-expressing metastasized neuroendocrine tumors, particularly gastroenteropancreatic. Reported toxicities include myelotoxicity and nephrotoxicity, the latter manifesting as decreased kidney function, often developing months to years after treatment completion. We present a case of PRRT-induced kidney toxicity manifesting as a severe Gitelman-like tubulopathy with preserved kidney function. Because profound hypokalemia and hypocalcemia can lead to life-threatening arrhythmias, we highlight the necessity for careful monitoring of serum and urine electrolytes in patients receiving PRRT.

Severe Metabolic Acidosis and Hepatopathy due to Leukoencephalopathy with Thalamus and Brainstem Involvement and High Lactate.

Leukoencephalopathy with thalamus and brainstem involvement and high lactate (LTBL) is a recently described autosomal recessive mitochondrial disease characterized by early onset of neurological symptoms, a biphasic clinical course, and distinctive neuroimaging. Pathogenic variants in the EARS2 gene that encode for mitochondrial glutamyl-tRNA synthetase are responsible for LTBL. Here, we describe the clinical course of an infant diagnosed with an acute crisis of LTBL and severe liver disease. This article illustrates the utility of blood lactate quantification in addition to basic metabolic testing and brain imaging in a child with low tone and poor growth. In addition, this case demonstrates the utility of current genetic diagnostic testing, in lieu of more invasive procedures, in obtaining rapid answers in this very complicated group of disorders.

Electrolyte and Mineral Homeostasis After Optimizing Early Macronutrient Intakes in VLBW Infants on Parenteral Nutrition.

OBJECTIVES: The aim of the present study was to evaluate electrolyte and mineral homeostasis in very-low-birth-weight (VLBW) infants who received high protein and energy intakes with a unique standardized parenteral nutrition solution containing electrolytes and minerals from birth onward. METHODS: Prospective cohort study in 102 infants with birth weight <1250 g. The evolution of plasma biochemical parameters was described during the first 2 weeks of life. RESULTS: During the first 3 days of life, mean parenteral intakes were 51 ±â€Š8 kcal · kg · day with 2.7 ±â€Š0.4 g · kg · day of protein, 1.1 ±â€Š0.2 mmol · kg · day of sodium and potassium, and 1.3 ±â€Š0.2 mmol · kg · day of calcium and phosphorus. Afterwards, most nutritional intakes (parenteral and enteral) met growth requirements. No infant developed a hyperkalemia >7 mmol/L, and a hypernatremia >150 mmol/L occurred only in 15.7% of the infants. In contrast, hyponatremia <130 mmol/L and hypokalemia <3 mmol/L occurred in 30.4% and 8.8% of the infants, respectively. The initial neonatal metabolic acidosis rapidly resolved in most infants and only 2.0% developed a base deficit >10 mmol/L after day 3 of life. Early hypocalcemia <1.8 mmol/L occurred in 13.7% of the infants. In contrast, hypophosphatemia <1.6 mmol/L occurred in 37.3% and hypercalcemia >2.8 mmol/L occurred in 12.7% of the infants. CONCLUSIONS: Increasing early protein and energy intakes in VLBW infants in the first week of life improves electrolyte homeostasis. It also increases the phosphorus requirements with a calcium-to-phosphorus ratio ≤1.0 (mmol/mmol) and the potassium and sodium requirements to avoid the development of a refeeding-like syndrome. These data suggest that the parenteral nutrition guidelines for VLBW infants for the first week of life need to be revised.

Update on inflammation in chronic kidney disease.

BACKGROUND: Despite recent advances in chronic kidney disease (CKD) and end-stage renal disease (ESRD) management, morbidity and mortality in this population remain exceptionally high. Persistent, low-grade inflammation has been recognized as an important component of CKD, playing a unique role in its pathophysiology and being accountable in part for cardiovascular and all-cause mortality, as well as contributing to the development of protein-energy wasting. SUMMARY: The variety of factors contribute to chronic inflammatory status in CKD, including increased production and decreased clearance of pro-inflammatory cytokines, oxidative stress and acidosis, chronic and recurrent infections, including those related to dialysis access, altered metabolism of adipose tissue, and intestinal dysbiosis. Inflammation directly correlates with the glomerular filtration rate (GFR) in CKD and culminates in dialysis patients, where extracorporeal factors, such as impurities in dialysis water, microbiological quality of the dialysate, and bioincompatible factors in the dialysis circuit play an additional role. Genetic and epigenetic influences contributing to inflammatory activation in CKD are currently being intensively investigated. A number of interventions have been proposed to target inflammation in CKD, including lifestyle modifications, pharmacological agents, and optimization of dialysis. Importantly, some of these therapies have been recently tested in randomized controlled trials. KEY MESSAGES: Chronic inflammation should be regarded as a common comorbid condition in CKD and especially in dialysis patients. A number of interventions have been proven to be safe and effective in well-designed clinical studies. This includes such inexpensive approaches as modification of physical activity and dietary supplementation. Further investigations are needed to evaluate the effects of these interventions on hard outcomes, as well as to better understand the role of inflammation in selected CKD populations (e.g., in children).

Coagulopathy induced by acidosis, hypothermia and hypocalcaemia in severe bleeding.

Acidosis, hypothermia and hypocalcaemia are determinants for morbidity and mortality during massive hemorrhages. However, precise pathological mechanisms of these environmental factors and their potential additive or synergistic anticoagulant and/or antiplatelet effects are not fully elucidated and are at least in part controversial. Best available evidences from experimental trials indicate that acidosis and hypothermia progressively impair platelet aggregability and clot formation. Considering the cell-based model of coagulation physiology, hypothermia predominantly prolongs the initiation phase, while acidosis prolongs the propagation phase of thrombin generation. Acidosis increases fibrinogen breakdown while hypothermia impairs its synthesis. Acidosis and hypothermia have additive effects. The effect of hypocalcaemia on coagulopathy is less investigated but it appears that below the cut-off of 0.9 mmol/L, several enzymatic steps in the plasmatic coagulation system are blocked while above that cut-off effects remain without clinical sequalae. The impact of environmental factor on hemostasis is underestimated in clinical practice due to our current practice of using routine coagulation laboratory tests such as partial thromboplastin time or prothrombin time, which are performed at standardized test temperature, after pH correction, and upon recalcification. Temperature-adjustments are feasible in viscoelastic point-of-care tests such as thrombelastography and thromboelastometry which may permit quantification of hypothermia-induced coagulopathy. Rewarming hypothermic bleeding patients is highly recommended because it improves patient outcome. Despite the absence of high-quality evidence, calcium supplementation is clinical routine in bleeding management. Buffer administration may not reverse acidosis-induced coagulopathy but may be essential for the efficacy of coagulation factor concentrates such as recombinant activated factor VII.

Fluid therapy in small ruminants and camelids.

Body water, electrolytes, and acid-base balance are important considerations in the evaluation and treatment of small ruminants and camelids with any disease process, with restoration of these a priority as adjunctive therapy. The goals of fluid therapy should be to maintain cardiac output and tissue perfusion, and to correct acid-base and electrolyte abnormalities. Hypoglycemia, hyperkalemia, and acidosis are the most life-threatening abnormalities, and require most immediate correction.

Treatment of metabolic acidosis in patients with stage 3 chronic kidney disease with fruits and vegetables or oral bicarbonate reduces urine angiotensinogen and preserves glomerular filtration rate.

Alkali therapy of metabolic acidosis in patients with chronic kidney disease (CKD) with plasma total CO2 (TCO2) below 22 mmol/l per KDOQI guidelines appears to preserve estimated glomerular filtration rate (eGFR). Since angiotensin II mediates GFR decline in partial nephrectomy models of CKD and even mild metabolic acidosis increases kidney angiotensin II in animals, alkali treatment of CKD-related metabolic acidosis in patients with plasma TCO2 over 22 mmol/l might preserve GFR through reduced kidney angiotensin II. To test this, we randomized 108 patients with stage 3 CKD and plasma TCO2 22-24 mmol/l to Usual Care or interventions designed to reduce dietary acid by 50% using sodium bicarbonate or base-producing fruits and vegetables. All were treated to achieve a systolic blood pressure below 130 mm Hg with regimens including angiotensin converting enzyme inhibition and followed for 3 years. Plasma TCO2 decreased in Usual Care but increased with bicarbonate or fruits and vegetables. By contrast, urine excretion of angiotensinogen, an index of kidney angiotensin II, increased in Usual Care but decreased with bicarbonate or fruits and vegetables. Creatinine-calculated and cystatin C-calculated eGFR decreased in all groups, but loss was less at 3 years with bicarbonate or fruits and vegetables than Usual Care. Thus, dietary alkali treatment of metabolic acidosis in CKD that is less severe than that for which KDOQI recommends therapy reduces kidney angiotensin II activity and preserves eGFR.

Changes in ruminal fermentation, milk performance and milk fatty acid profile in dairy cows with subacute ruminal acidosis and its regulation with pelleted beet pulp.

The aims of the experiment were to investigate the variation in ruminal fermentation, milk performance and milk fatty acid profile triggered by induced subacute ruminal acidosis (SARA); and to evaluate the ability of beet pulp (BP) as a replacement for ground maize in order to alleviate SARA. Eight Holstein-Friesian cows were fed four diets (total mixed rations) during four successive periods (each of 17 d): (1) without wheat (W0); (2) with 10% finely ground wheat (FGW) (W10); (3) with 20% FGW (W20); (4) with 20% FGW and 10% pelleted BP (BP10). Inducing SARA by diet W20 decreased the daily mean ruminal pH (6.37 vs. 5.94) and the minimum ruminal pH (5.99 vs. 5.41) from baseline to challenge period. Ruminal concentrations of total volatile fatty acid, propionate, butyrate, valerate and isovalerate increased with the W20 compared with the W0 and W10 treatments. The substitution of BP for maize increased the minimum ruminal pH and molar percentage of acetate and decreased the molar percentage of butyrate. The diets had no effect on dry matter intake (DMI) and milk yield, but the milk fat percentage and yield as well as the amount of fat-corrected milk was reduced in the W20 and BP10 treatments. The cows fed the W20 diet had greater milk concentrations of C11:0, C13:0, C15:0, C14:1, C16:1, C17:1, C18:2n6c, C20:3n6, total polyunsaturated fatty acids (FA) and total odd-chain FA, and lower concentrations of C18:0 and total saturated FA compared with the cows fed the W0 diet. Therefore, it can be concluded that changes in ruminal fermentation, milk fat concentration and fatty acid profile are highly related to SARA induced by feeding high FGW diets, and that the substitution of BP for maize could reduce the risk of SARA in dairy cows.

Does correction of metabolic acidosis slow chronic kidney disease progression?

PURPOSE OF REVIEW: Most patients with chronic kidney disease (CKD) have progressive decline in glomerular filtration rate (GFR), despite current treatment practices. Recent studies support that dietary acid reduction with oral sodium based alkali or base-inducing food types add kidney protection to that provided by current kidney-protective interventions. Related studies also support that correction of metabolic acidosis with dietary acid reduction slows CKD progression. We reviewed these recent studies that show improvement in CKD parameters and slower CKD progression in response to improvement of CKD-associated metabolic acidosis with these interventions. RECENT FINDINGS: Animal as well as human models of CKD show that alkali treatment ameliorates indices of kidney injury and also might slow GFR decline in patients with or without metabolic acidosis. These benefits have been similar with oral sodium-based alkali and base-inducing fruits and vegetables, supporting dietary acid reduction as an effective adjunct to conventional kidney-protective interventions. SUMMARY: Recent studies suggest that metabolic acidosis mediates nephropathy progression, and its treatment with the comparatively inexpensive and well tolerated intervention of dietary acid reduction holds promise to be an additional kidney-protective strategy in CKD management.