On the relationship between potassium and acid-base balance
In general, these anions are excreted with potassium and as a result, toluene ingestion maintained) and represents the difference between the commonly measured A pH severe acute acidosis with compromised hemodynamics is. Hyperkalemia is a common complication of acute kidney injury, particulary in . Measurement of the urinary uric acid:creatinine ratio may help differentiate. Resulting imbalances include acidosis (pH ), and high or low levels of key electrolyte ions, including sodium, potassium, calcium, They may be acute or chronic, may occur with varying degrees of severity, and may .. is recommended for monitoring treatment, but the difference should be noted.
Toxic ingestions are common causes of AG metabolic acidosis. The commonest causes are methanol and ethylene glycol intoxication. These alcohols are quickly absorbed from the GI tract. Peak serum levels are usually reached within hours. Immediately following ingestion, there is a large serum osmolar gap due to the presence of unmeasured, small, non-charge molecules. However, as these parent alcohols go through a two-step metabolism via alcohol dehydrogenase and aldehyde dehydrogenasethe osmolar gap resolves while an anion gap acidosis develops.
The toxicities mainly come from their metabolites. Formic acid is the final metabolite of methanol, and glycolate, glyoxylate and oxalate are end metabolites of ethylene glycol. However, because of slow hepatic metabolism, there is usually a latent period of hours before these toxicities manifest, especially if there is co-ingestion of alcohol which competitively inhibits alcohol dehydrogenase.
If treatment is not instituted, permanent damage may ensue. Both methanol and ethylene glycol are excreted primarily by the kidneys, though the lung contributes to some degree of methanol elimination. Salicylates can also cause AG metabolic acidosis. Salicylates are readily absorbed from the small intestine, and are metabolized in the liver through glycine conjugation. The amount of drug excreted unchanged in the urine is small, but can be dramatically increased with alkalization of urine due to trapping in the proximal tubule in a high pH environment preventing reabsorption.
A similar mechanism prevents movement of salicylates across the blood-brain barrier in the setting of an alkalosis reducing the neurotoxicity associated with this drug. This is important because many patients with salicylate ingestion have a respiratory alkalosis due to stimulation of the respiratory center and this should not be reversed as it is protective.
Mechanism of Hyperkalemia-Induced Metabolic Acidosis.
Similarly, carbonic anhydrase inhibitors, while they will increase urinary excretion of salicylic acid, are contraindicated because they lower extracellular pH and promote entry of the drug into the brain. The salicylic acid itself is not thought to be a significant contributor to the metabolic acidosis.
The mechanism for the AG metabolic acidosis in salicylate overdose is still unclear, but is thought to be secondary to inhibition of the Krebs cycle and subsequent accumulation of organic acids, e.
Inhalation of toluene can lead to both AG and NG metabolic acidosis. The AG is caused by the metabolite of toluene, hippuric acid.
Acid/Base Disorders: Metabolic Acidosis
However, hippuric acid is rapidly excreted in the urine and as the anion is exceted, the anion gap falls with a persistent NG acidosis. In general, these anions are excreted with potassium and as a result, toluene ingestion can lead to marked hypokalemia. It results from depletion of gluthathione. This prevents feedback inhibition of the gamma-glutamyl cycle and accumulation of oxoproline. It leads to an anion gap metabolic acidosis but may also cause a NG acidosis and hypokalemia due to rapid renal excretion of the anion.
It is usually seen in patients with chronic, high dose acetaminophen intake and particularly effects older women. Type A lactic acidosis is the most commonly seen in clinical practice and typically patients are hypotensive with obvious poor tissue perfusion.
Drugs associated with a Type B lactic acidosis include metformin, phenformin, nucleoside reverse transcriptase inhibitors and propofol. D-lactate is unique, as it is not metabolized by L-lactate dehydrogenase in human. It occurs in patients with short-bowel syndrome.
When the small bowel is bypassed, large amount of carbohydrates are delivered to the colon, where there is an abundance of gram-positive anaerobes e. Carbohydrates are metabolized into D-lactate which are then absorbed. In diabetic ketoacidosis, a NG metabolic acidosis is often encountered later in the course due to renal excretion of ketoacids.
This also explains the severe total body potassium deficit usually seen in these patients. Chronic kidney disease with decreased renal function is a common cause of metabolic acidosis. Patients usually manifest a NG metabolic acidosis due to decreased ammonium excretion.
Once renal function declines to a critical level, usually at late stage 4, acids from protein metabolism are retained, resulting in an AG metabolic acidosis. There are three major types of renal tubular acidosis RTA: Urine pH in these patients is typically above 5.
It stimulates bone resorption, and results in hypercalciuria and nephrocalcinosis. Hypokalemia is also common secondary to renal K wasting, and muscle weakness is a common complaint. Occasionally, an incomplete form of RTA-1 may occur. Common findings include NG acidosis and alkaline urine with hypocitraturia. However, patients with this incomplete form of RTA-1 are able to maintain serum bicarbonate levels unless stressed.
Urine pH in these cases can be variable. In the setting of an alkali load, the urine ph is elevated but under basal conditions, the urine pH is low. Mild hypokalemia is common. Type 4 RTA results from decreased aldosterone action either due to reduced hormone level or functional resistance. Urine pH commonly falls below 5.
The etiologies of RTA are summarized in Table 3. The history is an essential part of initial evaluation, though oftentimes, it is not available or simply unreliable. Histories from relatives and prehospital caregivers are important. Old patient records as well as details of recent hospitalization should be thoroughly reviewed. Differential diagnosis of AG metabolic acidosis Table 2. Differential diagnosis of NG metabolic acidosis Table 3. What tests to perform?Hyperkalemia: Causes, Effects on the Heart, Pathophysiology, Treatment, Animation.
First, measure arterial pH, PCO2, and serum bicarbonate concentration. Where a low bicarbonate is present, the anion gap should be checked to determine if this is a gap, non-gap or mixed disorder. The PCO2 will help determine whether there is a superimposed respiratory acidosis or alkalosis. The most common causes of hypercalcemia are primary hyperparathyroidism and malignancy e.
Chronic symptoms are more consistent with hyperparathyroidism, whereas recent onset of symptoms suggests malignancy the tumor is typically very advanced.
Signs and symptoms include renal stones typical of hyperparathyroidismlethargy, easy fatigue, depression, irritability, constipation, gastrointestinal symptoms e. Hypercalcaemia may be asymptomatic. Summary statement from a workshop on asymptomatic primary hyperparathyroidism: J Clin Endocrinol Metab. Magnesium deficiency can be caused by decreased magnesium intake from the diet, decreased magnesium absorption, or increased renal magnesium excretion renal magnesium wasting.
Acute Kidney Injury: Complications associated with Acute Kidney Injury
Symptoms are nonspecific and include: Primary hyperparathyroidism An endocrine disorder in which autonomous overproduction of parathyroid hormone PTH results in calcium metabolism derangement. Monoclonality and abnormal parathyroid hormone genes in parathyroid adenomas.
Diagnosis occurs through testing for a concurrent elevated serum calcium level and an inappropriately elevated intact serum PTH level. Nonsurgical management of primary hyperparathyroidism.
Complications due to primary PTH are uncommon and include osteoporosis and bone fracture due to leaching of calcium from bones, and renal calculi due to elevated serum and urine calcium. Innormocalcemic primary hyperparathyroidism was recognized as a variant of primary hyperparathyroidism and has yet to be thoroughly characterized.
Diabetic ketoacidosis Diabetic ketoacidosis DKA is an acute metabolic complication of diabetes that is potentially fatal and requires prompt medical attention for successful treatment.
DKA may be the initial presentation in people with newly diagnosed diabetes. Serum sodium, chloride, magnesium, and calcium are usually low, and the serum anion gap SAG; calculated by subtracting the sum of major measured anions, chloride and bicarbonate, from the major measured cation, sodiumserum potassium, BUN, and creatinine are usually elevated.
Venous pH, which is usually 0. Hyperglycemic crises in adult patients with diabetes. Urinary tract infections and pneumonia are the most common infections reported. Hyperglycemic crises in diabetes mellitus type 2. Endocrinol Metab Clin North Am. Distal renal tubular acidosis and the potassium enigma. In the absence of other acid-base disorders the serum anion gap SAG; calculated by subtracting the sum of major measured anions, chloride and bicarbonate, from the major measured cation, sodium is normal.
Proximal and classic distal RTA are characterized by hypokalemia. J Am Soc Nephrol. Serum sodium is usually normal. RTA is rarely symptomatic. Patients with severe acidemia can show hyperventilation or Kussmaul breathing due to respiratory compensation. Symptomatic hypocalcemia requires treatment with intravenous calcium, however the aggressiveness of therapy may need to be tempered in the setting of concomitant severe hyperphosphatemia, as calcium infusion may result in metastatic calcium phosphate deposition.
It is unusual for hypercalcemia to develop as a consequence of AKI. More commonly, when hypercalcemia is present in the setting of AKI, both are a consequence of an underlying disease, such as multiple myeloma, or the AKI is mediated in part by the hypercalcemia. Hypercalcemia may develop during the recovery from myoglobinuric AKI in rhabdomyolysis as calcium deposited in injured muscle is mobilized. Mild asymptomatic hypermagnesemia is common in oliguric AKI as the result of impaired excretion of ingested magnesium.
More severe hypermagnesemia is usually iatrogenic, as the result of parenteral administration, as in the management of AKI associated with pre-eclampsia. Hypomagnesemia may complicate non-oliguric nephrotoxic AKI associated with aminoglycosides, cisplatin and amphotericin B.
Acid/Base Disorders: Metabolic Acidosis - Renal and Urology News
Renal magnesium wasting may persist even after renal function has recovered. Mild hyperuricemia, as a result of decreased renal uric acid excretion, is common in AKI. More severe elevations in serum uric acid develop when AKI develops in the setting of hypercatabolism or cell lysis. In the setting of tumor lysis syndrome, acute urate nephropathy underlies the development of AKI.
Measurement of the urinary uric acid: Gastrointestinal and Nutritional Complications The major gastrointestinal complications associated with acute kidney injury include anorexia, nausea and vomiting and upper gastrointestinal bleeding, primarily due to stress ulcers and gastritis. Acute kidney injury is recognized as a hypercatabolic state, however the precise mechanism for the hypercatabolic state is not known.
A variety of factors including the hypercatabolic nature of underlying disorders eg, sepsis, rhabdomyolysis, trauma ; hormonal disturbances including elevated levels of glucagon, catecholamines, growth hormone and cortisol and insulin resistance; and acute uremia per se, which has been associated with accumulation of proteases in the blood.