diabetestalk.net

Renal Tubular Acidosis Treatment

Distal Renal Tubular Acidosis

Distal Renal Tubular Acidosis

I do not know why anyone would diagnose distal RTA (dRTA) very often. As I will show you it has colorful and unusual characteristics as unmistakable as rare, so diagnosis is not difficult. But many more people think they have than have it. In my 50 years of kidney stone prevention I have perhaps a few dozen examples or so, out of many thousands of stone formers. This is another of those long, elaborate articles only the most devoted read. Even so, elaborate as it is, this article tells only part of the story. It simplifies or simply ignores the mechanism for low potassium in dRTA, and left for another time its genetic causes, and also the bone and mineral disorders and treatment outcomes. I forgive myself, as just this part has been most taxing to write and is equally so to read. In a subsequent article I hope to expand on diagnosis and treatment, the bone and mineral disorders, genetic transporter disorders, and take up the novel modern issue of acid retention and its effects on kidneys. So consider the present article a part of my planned contribution. The featured illustration of kidney tissue from a patient with dRTA shows many crystal deposits on a radiograph (panel a), that at surgery mostly are calcified deposits (panel b) that nearly replace papillary tissue (panels c and d). Kidneys make urine more acid than blood because most of us eat a diet that imposes an acid load on the body and kidneys need to remove that acid.But apart from balancing acid excretion to diet acid load, unless kidneys acidify urine calcium phosphate crystals may form in such profusion as to block kidney tubules and produce kidney stones. This happens because as they conserve water kidneys concentrate urine calcium phosphate salts far above their levels in blood. If they simultaneously mak Continue reading >>

Renal Tubular Acidosis

Renal Tubular Acidosis

Renal tubular acidosis (RTA) is a disease that occurs when the kidneys fail to excrete acids into the urine, which causes a person's blood to remain too acidic. Without proper treatment, chronic acidity of the blood leads to growth retardation, kidney stones, bone disease, chronic kidney disease, and possibly total kidney failure. The body's cells use chemical reactions to carry out tasks such as turning food into energy and repairing tissue. These chemical reactions generate acids. Some acid in the blood is normal, but too much acidacidosiscan disturb many bodily functions. Healthy kidneys help maintain acid-base balance by excreting acids into the urine and returning bicarbonatean alkaline, or base, substanceto the blood. This "reclaimed" bicarbonate neutralizes much of the acid that is created when food is broken down in the body. The movement of substances like bicarbonate between the blood and structures in the kidneys is called transport. One researcher has theorized that Charles Dickens may have been describing a child with RTA in the character of Tiny Tim from A Christmas Carol. Tiny Tim's small stature, malformed limbs, and periods of weakness are all possible consequences of the chemical imbalance caused by RTA.1 In the story, Tiny Tim recovers when he receives medical treatment, which would likely have included sodium bicarbonate and sodium citrate, alkaline agents to neutralize acidic blood. The good news is that medical treatment can indeed reverse the effects of RTA. To diagnose RTA, doctors check the acid-base balance in blood and urine samples. If the blood is more acidic than it should be and the urine less acidic than it should be, RTA may be the reason, but additional information is needed to rule out other causes. If RTA is the reason, additional in Continue reading >>

Renal Tubular Acidosis

Renal Tubular Acidosis

Patients with renal tubular acidosis (RTA) are often asymptomatic but may present with complaints of muscular weakness related to associated hypokalemia. Patients with severe acidemia can show hyperventilation or Kussmaul breathing due to respiratory compensation. Patients with RTA have a low arterial pH and serum bicarbonate with hyperchloremia and a normal serum anion gap. The urine pH exceeds 5.5 in classic distal RTA, but is lower than 5.0 in patients with untreated proximal RTA and is low also in hyperkalemic distal RTA. Alkali therapy is the mainstay of treatment. Potassium supplementation may be required for hypokalemia, and low-potassium diets are used if hyperkalemia is present. If hyperkalemic distal RTA is due to mineralocorticoid deficiency, fludrocortisone can be given unless it is contraindicated due to the presence of fluid overload or uncontrolled hypertension. Proximal RTA occurs most often as a component of Fanconi syndrome, which is characterized by generalized dysfunction of the proximal tubule, with the resultant urinary loss of bicarbonate, calcium, phosphate, urate, amino acids, glucose, and other organic acids and bases. In children, Fanconi syndrome causes growth retardation, renal rickets, and severe metabolic acidosis. Adult cases exhibit similar urinary losses, but the clinical impact is largely restricted to metabolic acidosis. Fanconi syndrome is marked by the appearance in the urine of all amino acids. Specific amino aciduria as seen in isolated cystinuria, glucose loss in isolated glycosuria, and isolated phosphaturia do not constitute Fanconi syndrome. The term renal tubular acidosis (RTA) describes any one of a number of disorders, in which the excretion of fixed acid (distal RTA) or the reabsorption of filtered bicarbonate (proximal R Continue reading >>

Orphanet: Distal Renal Tubular Acidosis

Orphanet: Distal Renal Tubular Acidosis

Only comments seeking to improve the quality and accuracy of information on the Orphanet website are accepted. For all other comments, please send your remarks via contact us . Only comments written in English can be processed. Check this box if you wish to receive a copy of your message Distal renal tubular acidosis (dRTA) is a disorder of impaired net acid secretion by the distal tubule characterized by hyperchloremic metabolic acidosis. The classic form is often associated with hypokalemia whereas other forms of acquired dRTA may be associated with hypokalemia, hyperkalemia or normokalemia. Inheritance: Autosomal dominantorAutosomal recessiveorNot applicable Prevalence of dRTA is unknown but is often underreported. The hereditary forms of dRTA are more prevalent in areas of high consanguinity (Arabic peninsula and North Africa) whereas acquired dRTA has been reported more frequently in Western countries. Disease onset can occur at any age, depending on cause. Hereditary dRTA subtypes include autosomal dominant (AD) and autosomal recessive (AR) dRTA (see these terms). A recessive subtype of dRTA associated with anemia has also been described in Southeast Asia. AR forms are frequently diagnosed in infants and young children. AD dRTA is mostly diagnosed in adolescents and young adults. Patients with dRTA can be asymptomatic or can present with polyuria, polydipsia, weakness and fatigue (symptoms associated with hypokalemia). Failure to thrive, rickets, stunting of growth (seen in children) and osteomalacia or osteopenia (seen in adults) are a result of urinary calcium wastage and a loss of calcium salts from the bones. Hypercalciuria, nephrolithiasis and nephrocalcinosis usually occur. Low plasma potassium levels in those with the classic form of dRTA can also cause ca Continue reading >>

Renal Tubular Acidosis

Renal Tubular Acidosis

Renal tubular acidosis (RTA) is acidosis and electrolyte disturbances due to impaired renal hydrogen ion excretion (type 1), impaired bicarbonate resorption (type 2), or abnormal aldosterone production or response (type 4). (Type 3 is extremely rare and is not discussed.) Patients may be asymptomatic, display symptoms and signs of electrolyte derangements, or progress to chronic kidney disease. Diagnosis is based on characteristic changes in urine pH and electrolytes in response to provocative testing. Treatment corrects pH and electrolyte imbalances using alkaline agents, electrolytes, and, rarely, drugs. RTA defines a class of disorders in which excretion of hydrogen ions or reabsorption of filtered bicarbonate is impaired, leading to a chronic metabolic acidosis with a normal anion gap. Hyperchloremia is usually present, and secondary derangements may involve other electrolytes, such as potassium (frequently) and calcium (rarelysee Table: Some Features of Different Types of Renal Tubular Acidosis* ). Chronic RTA is often associated with structural damage to renal tubules and may progress to chronic kidney disease . Some Features of Different Types of Renal Tubular Acidosis* Treatment of concomitant abnormalities related to potassium, calcium, and phosphate metabolism Treatment consists of correction of pH and electrolyte balance with alkali therapy. Failure to treat RTA in children slows growth. Alkaline agents such as sodium bicarbonate, potassium bicarbonate, or sodium citrate help achieve a relatively normal plasma bicarbonate concentration (22 to 24 mEq/L). Potassium citrate can be substituted when persistent hypokalemia is present or, because sodium increases calcium excretion, when calcium calculi are present. Vitamin D (eg, ergocalciferol 800 IU po once/day) Continue reading >>

Renal Tubular Acidosis: Symptoms & Treatment

Renal Tubular Acidosis: Symptoms & Treatment

Renal Tubular Acidosis: Symptoms & Treatment Watch short & fun videos Start Your Free Trial Today Log in or sign up to add this lesson to a Custom Course. Custom Courses are courses that you create from Study.com lessons. Use them just like other courses to track progress, access quizzes and exams, and share content. Organize and share selected lessons with your class. Make planning easier by creating your own custom course. Create a new course from any lesson page or your dashboard. Click "Add to" located below the video player and follow the prompts to name your course and save your lesson. Click on the "Custom Courses" tab, then click "Create course". Next, go to any lesson page and begin adding lessons. Edit your Custom Course directly from your dashboard. Name your Custom Course and add an optional description or learning objective. Create chapters to group lesson within your course. Remove and reorder chapters and lessons at any time. Share your Custom Course or assign lessons and chapters. Share or assign lessons and chapters by clicking the "Teacher" tab on the lesson or chapter page you want to assign. Students' quiz scores and video views will be trackable in your "Teacher" tab. You can share your Custom Course by copying and pasting the course URL. Only Study.com members will be able to access the entire course. Renal tubular acidosis (RTA) is a condition in which the kidneys don't filter enough acid out of the bloodstream, causing the blood to become too acidic. This lesson will discuss the symptoms of RTA, and talk about different treatment options. Kevin has always been pretty healthy, but suddenly in his 30's, he began experiencing kidney stones. They were extremely painful and he couldn't figure out what kept causing them, so he went to his doctor to ha Continue reading >>

Renal Tubular Acidosis Symptoms And Treatments

Renal Tubular Acidosis Symptoms And Treatments

It is a disorder that may be inherited or a symptom of an underlying disease. Experts believe that this type of RTA is caused by abnormal genes, although in most occasions it occurs due to systemic diseases such as lupus and Sjgrens syndrome.Other conditions and diseases associated with Type 1 RTA include analgesic nephropathy, chronic active hepatitis, hereditary deafness, hyperparathyroidism, hyperthyroidism, primary biliary cirrhosis, and sickle cell anemia. Classical distal RTA is also associated with chronic urinary tract infections, obstructive uropathy, rejection of a transplanted kidney, and renal medullary cystic disease. Most of these conditions and diseases cause abnormal calcium deposits build up in the kidney and impairment of the distal tubule function. Another consequence of Type 1 RTA is low levels of potassium , which results from excess excretion of potassium into the urine by the kidneys instead of returning it to the bloodstream. Renal tubular acidosis symptoms associated with inadequate potassium levels include muscle paralysis, irregular heartbeat, weakness or even death. It is common in children and occurs as part of Fanconis syndrome. Proximal renal tubular acidosis symptoms include abnormal excretion of amino acids, glucose, phosphate, and citrate into the urine. Other symptoms include low potassium levels in the blood and vitamin D deficiency . Type 2 RTA can also develop from hereditary disorders that interfere with normal breakdown and utilization of nutrients in the body. Among such disorders include Wilson disease, hereditary fructose intolerance, and cystinosis disease. It is common in patients being treated with a chemotherapy drug called ifosfamide. Other drugs such as tetracycline and acetazolamide can also lead to the disorder. Proxim Continue reading >>

Renal Tubular Acidosis: The Clinical Entity

Renal Tubular Acidosis: The Clinical Entity

Renal Tubular Acidosis: The Clinical Entity Department of Pediatrics, Hospital de Cruces, Vizcaya, Spain. Correspondence to Professor J. Rodrguez-Soriano, Department of Pediatrics, Hospital de Cruces, Plaza de Cruces s/n, Baracaldo, 48903 Vizcaya, Spain. Phone: 34-94-6006357; Fax: 34-94-6006044; E-mail: jsoriano{at}hcru.osakidetza.net The term renal tubular acidosis (RTA) is applied to a group of transport defects in the reabsorption of bicarbonate (HCO3), the excretion of hydrogen ion (H+), or both. This condition was first described in 1935 ( 1 ), confirmed as a renal tubular disorder in 1946 ( 2 ), and designated renal tubular acidosis in 1951 ( 3 ). The RTA syndromes are characterized by a relatively normal GFR and a metabolic acidosis accompanied by hyperchloremia and a normal plasma anion gap. In contrast, the term uremic acidosis is applied to patients with low GFR in whom metabolic acidosis is accompanied by normo- or hypochloremia and an increased plasma anion gap. The renal acid-base homeostasis may be broadly divided into two processes: (1) reabsorption of filtered HCO3, which occurs fundamentally in the proximal convoluted tubule; and (2) excretion of fixed acids through the titration of urinary buffers and the excretion of ammonium, which takes place primarily in the distal nephron. The mechanisms for proximal reabsorption of approximately 80 to 90% of filtered HCO3 are displayed in Figure 1 . The foremost processes occurring in this segment are H+ secretion at the luminal membrane via a specific Na+- H+ exchanger (NHE-3) and HCO3 transport at the basolateral membrane via a Na+- HCO3 cotransporter (NBC-1). In the proximal tubules, carbonic acid (H2CO3) is formed within the cell by the hydration of CO2, a reaction catalyzed by a soluble cytoplasmic carbonic Continue reading >>

Renal Tubular Acidosis And Uraemic Acidosis

Renal Tubular Acidosis And Uraemic Acidosis

Metabolic acidosis can occur in both acute and chronic renal disorders the anion gap may be elevated, due to uraemic acidosis the anion gap may be normal, due to renal tubular acidosis (RTA) Uraemic acidosis results from the loss of functional nephrons decreased glomerular filtration rate (GFR) (e.g. <20 mL/min) accumulation of acidic anions such as phosphate and sulfate occurs causes high anion gap metabolic acidosis (HAGMA) patients manifest as renal failure, often have prolonged survival and develop chronic complications such as bone demineralisation Renal tubular acidosis (RTA) involves defects isolated to the renal tubules only GFR may be normal or only minimally affected primary problem is defective renal acid-base regulation due to impaired ability to acidify the urine and excrete acid results in net acid retention and hyperchloremic normal anion gap metabolic acidosis (NAGMA) may be incomplete and only develop in the presence of an acid load occurs despite a normal or only mildly reduced glomerular filtration rate (GFR) RTA is often detected incidentally through an abnormal blood workup, but some patients present with clinical features such as poor growth, dehydration, or altered mental state COMPARISON OF TYPES OF RENAL TUBULAR ACIDOSIS (RTA) urine pH remains >5.5 despite severe acidaemia (HCO3 < 15mmol/L) HCO3loading test leads to increased urinary HCO3 may require an acid load test to see whether urinary pH remains > 5.5 hyperchloraemic acidosis, alkaline urine, and renal stone formation secondary hyperaldosteronism results in increased K+ loss in urine NaHCO3 (corrects Na+ deficit, ECF volume and corrects hypokalaemia) sodium and potassium citrate solutions can be useful if hypokalaemia persistent citrate also binds Ca2+ in the urine and can help to prevent Continue reading >>

Renal Tubular Acidosis

Renal Tubular Acidosis

Each time our internal organs do something, such as digesting food or healing damaged tissue, chemical reactions take place in the body's cells. These reactions cause acid to go into the bloodstream. Normally, the kidneys remove excess acid from blood, but certain diseases, genetic defects, or drugs can damage a kidney's ability to do this important job. This can allow too much acid to build up in the blood and cause problems. When this happens, it's called renal tubular acidosis (RTA). Without treatment, RTA can affect a child's growth and cause kidney stones , fatigue, muscle weakness, and other symptoms. Over time, untreated acidosis can lead to long-term problems like bone disease, kidney disease , and kidney failure. Fortunately, such complications are rare, since most cases of RTA can be effectively treated with medicines or by treating the condition that's causing the acid to build up. The kidneys are a pair of bean-shaped organs located toward the back of the abdominal cavity, just above the waist. The kidneys remove waste products and extra water from the food a person eats, returning chemicals the body needs (such as sodium, phosphorus, and potassium) back into the bloodstream. The extra water combines with other waste to become urine (pee). The main functional units of the kidneys, where the blood filtering happens, are tiny structures called nephrons. Each kidney has about a million nephrons, and each nephron has a renal tubule, a tube where the acid and waste products filtered from the blood are secreted into urine. Having a disease or defect can interfere with how the renal tubules function, which can lead to RTA. There are a few different kinds of RTA. The first two types are named for the part of the renal tubule in which the damage or defect is found. Continue reading >>

Successful Management Of Refractory Type 1 Renal Tubular Acidosis With Amiloride

Successful Management Of Refractory Type 1 Renal Tubular Acidosis With Amiloride

Successful Management of Refractory Type 1 Renal Tubular Acidosis with Amiloride 1Department of Internal Medicine, University of Maryland School of Medicine, Baltimore, MD, USA 2Division of Nephrology, University of Maryland Medical Center Midtown Campus, Baltimore, MD, USA 3Department of Medicine, Division of Nephrology, Johns Hopkins School of Medicine, Baltimore, MD, USA 4Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, USA 5Nephrology Center of Maryland, Baltimore, MD, USA Correspondence should be addressed to Patrick Oguejiofor ; [email protected] Received 14 July 2016; Revised 2 December 2016; Accepted 14 December 2016; Published 3 January 2017 Copyright 2017 Patrick Oguejiofor et al. This is an open access article distributed under the Creative Commons Attribution License , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. A 28-year-old female with history of hypothyroidism, Sjgrens Syndrome, and Systemic Lupus Erythematosus (SLE) presented with complaints of severe generalized weakness, muscle pain, nausea, vomiting, and anorexia. Physical examination was unremarkable. Laboratory test showed hypokalemia at 1.6 mmol/l, nonanion metabolic acidosis with HCO3 of 11 mmol/l, random urine pH of 7.0, and urine anion gap of 8 mmol/l. CT scan of the abdomen revealed bilateral nephrocalcinosis. A diagnosis of type 1 RTA likely secondary to Sjgrens Syndrome was made. She was started on citric acid potassium citrate with escalating dosages to a maximum dose of 60 mEq daily and potassium chloride over 5 years without significant improvement in serum K+ and HCO3 levels. She had multiple emergency room visits for persistent muscle pain, generalized weakness, Continue reading >>

Distal Renal Tubular Acidosis

Distal Renal Tubular Acidosis

Distal renal tubular acidosis (dRTA) or Type 1 renal tubular acidosis (RTA) is the classical form of RTA, being the first described. Distal RTA is characterized by a failure of acid secretion by the alpha intercalated cells of the cortical collecting duct of the distal nephron . This failure of acid secretion may be due to a number of causes, and it leads to an inability to acidify the urine to a pH of less than 5.3. Radiograph of a rickets sufferer, a complication of both distal and proximal RTA. Because renal excretion is the primary means of eliminating acid from the body, there is consequently a tendency towards acidemia . This leads to the clinical features of dRTA: [1] Urinary stone formation (related to alkaline urine, hypercalciuria , and low urinary citrate). [2] Nephrocalcinosis (deposition of calcium in the substance of the kidney) Bone demineralisation (causing rickets in children and osteomalacia in adults) The symptoms and sequelae of dRTA are variable and range from being completely asymptomatic , to loin pain and hematuria from kidney stones , to failure to thrive and severe rickets in childhood forms as well as possible renal failure and even death. dRTA commonly leads to sodium loss and volume contraction, which causes a compensatory increase in blood levels of aldosterone . [3] Aldosterone causes increased resorption of sodium and loss of potassium in the collecting duct of the kidney, so these increased aldosterone levels cause the hypokalemia which is a common symptom of dRTA. [3] The pH of patient's blood is highly variable, and acidemia is not necessarily characteristic of sufferers of dRTA at any given time. One may have dRTA caused by alpha intercalated cell failure without necessarily being acidemic; termed incomplete dRTA, which is characteri Continue reading >>

Renal Tubular Acidosis (rta)

Renal Tubular Acidosis (rta)

Renal Tubular Acidosis (RTA) is a disease of the kidneys Namely the renal tubules. There are three main types of renal tubular acidosis Type one, type two, and type four. Type three renal tubular acidosis is a term no longer used for its defining feature resolved with age and was not part of the pathological process. The type of RTA is assigned depending on which part of the acid handling mechanism is affected. Statistics on Renal Tubular Acidosis (RTA) There are no widely accepted statistics on the rate of RTA. The disease, however, does occur at any age and afflicts men more so than women. Risk Factors for Renal Tubular Acidosis (RTA) Type 1 This condition may be inherited or acquired. In the majority of cases, this form of RTA results from the presence of another disease such as Sjogrens syndrome , hypergammaglobulinaemia, chronic active hepatitis and systemic Lupus Erythematosus. Type 2 This condition may also be inherited or acquired. The pattern of inheritance in this condition is more unpredicyable than that of type 1 RTA. This condition may also be present in associated with other disease states such as Fanconi Syndrome and can be induced by certain drugs such as acetazolamide. Type 4 This condition cannot be inherited and is exclusively acquired. It occurs in patients with poor kidney function and may arise or be made worse with the use of drugs such as trimethoprim, anti-inflammatory drugs, ACE inhibitors and heparin. Progression of Renal Tubular Acidosis (RTA) This condition causes prolonged blood acidity increasing the breakdown of calcium within the bony skeleton of the body. This increases the concentration of calcium within the bloodstream. More calcium is therefore allowed to enter the kidneys. In the presence of blood acidity, the kidneys are unable to Continue reading >>

Renal Tubular Acidosis (rta)

Renal Tubular Acidosis (rta)

By L. Aimee Hechanova, MD, Assistant Professor of Medicine, Texas Tech University; Attending Nephrologist, University Medical Center (See also Introduction to Disorders of Kidney Tubules .) In renal tubular acidosis, the kidney tubules malfunction, resulting in excess levels of acid in the blood. The tubules of the kidneys that remove acid from the blood are damaged when a person takes certain drugs or has another disorder that affects the kidneys. Often muscle weakness and diminished reflexes occur when the disorder has been present for a long time. Blood tests show high acid levels and a disturbance of the body's acid-base balance. Some people drink a solution of baking soda every day to neutralize the acid. To function normally, body acids and alkali (such as bicarbonate) must be balanced. Normally, the breakdown of food produces acids that circulate in the blood. The kidneys remove acids from the blood and excrete them in the urine. This function is predominantly carried out by the kidney tubules . In renal tubular acidosis, the kidney tubules malfunction in one of two ways that tend to increase acids in the blood ( metabolic acidosis ): Too little of the acids the body produces are excreted, so acid levels in blood increase. Too little of the bicarbonate that filters through the kidney tubules is reabsorbed, so too much bicarbonate is lost in the urine. In renal tubular acidosis, the balance of electrolytes is also affected. Renal tubular acidosis may lead to the following problems: Low or high potassium levels in the blood Calcium deposits in the kidneys, which may lead to kidney stones Painful softening and bending of the bones (osteomalacia or rickets ) Renal tubular acidosis may be a permanent, inherited disorder in children. However, it may be an intermittent Continue reading >>

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic Acidosis Treatment & Management: Approach Considerations, Type 1 Renal Tubular Acidosis, Type 2 Renal Tubular Acidosis

Metabolic AcidosisTreatment & Management Author: Christie P Thomas, MBBS, FRCP, FASN, FAHA; Chief Editor: Vecihi Batuman, MD, FASN more... Treatment of acute metabolic acidosis by alkali therapy is usually indicated to raise and maintain the plasma pH to greater than 7.20. In the following two circumstances this is particularly important. When the serum pH is below 7.20, a continued fall in the serum HCO3- level may result in a significant drop in pH. This is especially true when the PCO2 is close to the lower limit of compensation, which in an otherwise healthy young individual is approximately 15 mm Hg. With increasing age and other complicating illnesses, the limit of compensation is likely to be less. A further small drop in HCO3- at this point thus is not matched by a corresponding fall in PaCO2, and rapid decompensation can occur. For example, in a patient with metabolic acidosis with a serum HCO3- level of 9 mEq/L and a maximally compensated PCO2 of 20 mm Hg, a drop in the serum HCO3- level to 7 mEq/L results in a change in pH from 7.28 to 7.16. A second situation in which HCO3- correction should be considered is in well-compensated metabolic acidosis with impending respiratory failure. As metabolic acidosis continues in some patients, the increased ventilatory drive to lower the PaCO2 may not be sustainable because of respiratory muscle fatigue. In this situation, a PaCO2 that starts to rise may change the plasma pH dramatically even without a significant further fall in HCO3-. For example, in a patient with metabolic acidosis with a serum HCO3- level of 15 and a compensated PaCO2 of 27 mm Hg, a rise in PaCO2 to 37 mm Hg results in a change in pH from 7.33 to 7.20. A further rise of the PaCO2 to 43 mm Hg drops the pH to 7.14. All of this would have occurred whi Continue reading >>

More in ketosis