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What Is Distal Renal Tubular Acidosis?

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 >>

Distal Renal Tubular Acidosis

Distal Renal Tubular Acidosis

Distal renal tubular acidosis is a disease of defective urinary acidification, which is caused by insufficient net acid excretion by the kidney. Fiona E. Karet, in Genetic Diseases of the Kidney , 2009 Distal renal tubular acidosis is a disease of defective urinary acidification, which is caused by insufficient net acid excretion by the kidney. Unfortunately, the classification of the RTAs can be confusing, because within the overall historical scheme of nomenclature, types 1 and 4 RTA are both caused by distal nephron dysfunction. In this chapter we are mainly concerned with type 1 RTA, which is directly due to dysfunction of the acid-handling -intercalated cells (-IC) in the collecting system, and this distal form is associated with hypokalemia. In contrast, type 4 RTA is associated with hypoaldosteronism (true and pseudo-) and defective distal nephron sodium handling by principal cells in this same nephron segment, and therefore with hyperkalemia, and only secondarily with inadequate acid excretion. Both types 1 and 4 dRTA actually cover large groups of different conditions, both inherited and acquired. Thus it is type 1 RTA that is most commonly referred to as distal RTA (dRTA). Julian L. Seifter, in Goldman's Cecil Medicine (Twenty Fourth Edition) , 2012 In distal renal tubular acidosis (type 1), failure to produce ammonia leads to an inability to excrete net acid, thereby leading to continuous retention of acid in the body. The degree of acidemia is often severe, with pH reaching values as low as 7.2, whereas urine pH usually exceeds 5.3. Kindreds have been described in which mutations in genes for the distal vacuolar H+-ATPase cause an autosomal recessive distal renal tubular acidosis with deafness. Mutations resulting in defective Cl/HCO3 exchange protein (AE1) Continue reading >>

Omim Entry - # 602722 - Renal Tubular Acidosis, Distal, Autosomal Recessive; Rtadr

Omim Entry - # 602722 - Renal Tubular Acidosis, Distal, Autosomal Recessive; Rtadr

A number sign (#) is used with this entry because autosomal recessive distal renal tubular acidosis (dRTA) with preserved hearing or late-onset sensorineural hearing loss is caused by homozygous mutation in the ATP6N1B gene (ATP6V0A4; 605239 ) on chromosome 7q34. The maintenance of body fluid pH within a narrow range is critical for a wide variety of essential biochemical and metabolic functions. The kidney plays a key role in this homeostasis under normal circumstances, owing to its ability to vary bicarbonate reclamation and net acid excretion over a wide range. In the renal tubular acidoses (RTAs), however, acid-base balance becomes deranged either because of inability to secrete acid in the distal nephron or because of proximal bicarbonate loss ( 267200 ). Primary distal RTA is characterized by the failure of the kidney to produce an appropriately acid urine in the presence of systemic metabolic acidosis or after acid loading, due to failure of hydrogen ion secretion or bicarbonate reabsorption in the distal nephron. This results in hyperchloremic metabolic acidosis of varying severity. The condition is usually accompanied by nephrocalcinosis or nephrolithiasis. Other findings include hypokalemia and normal serum calcium and phosphate levels, although osteomalacia or rickets may supervene in untreated cases. Alkali replacement serves to reverse most of the biochemical abnormalities. Both autosomal dominant ( 179800 ) and autosomal recessive patterns have been observed in kindreds with primary distal RTA, and the spectrum of clinical severity is wide. Some patients with autosomal dominant distal RTA remain asymptomatic until adolescence or adulthood, whereas others, and those with recessive disease, may be severely affected in infancy, with impaired growth and early 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 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 >>

Primary Distal Renal Tubular Acidosis: Novel Findings In Patients Studied By Next-generation Sequencing

Primary Distal Renal Tubular Acidosis: Novel Findings In Patients Studied By Next-generation Sequencing

Primary distal renal tubular acidosis: novel findings in patients studied by next-generation sequencing Pediatric Research volume79,pages496501(2016) Cite this article A Corrigendum to this article was published on 01 November 2017 Primary distal renal tubular acidosis (DRTA) is a rare disease caused by loss-of-function mutations in at least three genes (ATP6V0A4, ATP6V1B1, and SLC4A1) involved in urinary distal acidification. The next-generation sequencing (NGS) technique facilitates the search for mutations in DRTA patients and helps to characterize the genetic and clinical spectrum of the disease. Ten DRTA patients were studied. They had normal serum anion gap (AG), metabolic acidosis with simultaneous positive urinary AG, and inability to maximally acidify the urine. The exons of the three genes were sequenced in two pools by ultrasequencing. Putative mutations were confirmed by corresponding Sanger sequencing of each exon. We found 13 mutations in nine patients. ATP6V0A4: Intron16+2insA; p.R807Q; p.Q276fs; p.P395fs; Intron7-2T>C. ATP6V1B1: p.I386fs; p.R394Q. SLC4A1: p.V245M; p.R589C; p.R589H; p.G609A. One case was a compound heterozygous with a known mutation in ATP6V1B1 (p.G609R) and a pathogenic variation at SLC4A1 (p.E508K). One patient was negative for mutations. This study evidences that NGS is labor and cost effective for the analysis of DRTA genes. Our results show for the first time SLC4A1 gene mutations in Spanish patients and disclose that compound heterozygosity at two different genes can be responsible for DRTA. Primary distal renal tubular acidosis (DRTA) ( 1 ) is caused by a genetic defect that impairs the ability of kidneys to maximally acidify the urine in the presence of normal serum anion gap hyperchloremic metabolic acidosis. Autosomal-recessive Continue reading >>

Type 1 (distal) Renal Tubular Acidosis - Deranged Physiology

Type 1 (distal) Renal Tubular Acidosis - Deranged Physiology

This form of renal tubular acidosis is a failure of the cortical collecting duct to decrease chloride resorption in response to acidosis. The defect seems to be in the activity of alpha-intercalated cells of the collecting duct. The mechanism of distal renal tubular acidosis There are a few mechanisms discussed in the literature, each of which can result in a diminished urinary acidification, and in a normal anion gap metabolic acidosis. The key feature of the renal tubular mechanisms involved here is the import of systemic ammonia, as well as the de novo synthesis of ammonia from glutamine within the renal tubule. (This ammonia also leaks out of the kidney into the systemic circulation, but in itself it is not a significant contributor to systemic ammonia levels , in case you are wondering.) Firstly, one can completely destroy the water-impermeable membranes which separate the peritubular capillary and the tubular lumen. This would lead to an equilibration of bicarbonate and chloride, with the resulting failure to excrete one and retain the other. This is exactly what happens when amphotericin attacks the tubule. Any interference with NH3 and H+ excretion in the alpha-intercalated cells is another such mechanism. The ionized NH4+, the combination of excreted NH3 and H+ remains in the lumen of the tubule (where it is trapped by its charge). This positive charge is balanced by the chloride anions, which are already present in the tubule. Any defect of ammonia excretion would therefore decrease the concentration of chloride anions in the tubular fluid. This chloride would have to be retained. The main defect in this case seems to be a problem with ATP-powered H+ secretion, which is normally an acidity-regulated process. As pH drops, so the activity of this protein should Continue reading >>

Distal Renal Tubular Acidosis Sequencing Panel - Preventiongenetics

Distal Renal Tubular Acidosis Sequencing Panel - Preventiongenetics

Distal Renal Tubular Acidosis Sequencing Panel We are happy to accommodate requests for single genes or a subset of these genes. The price will remain the list price. If desired, free reflex testing to remaining genes on panel is available. Alternatively, a single gene or subset of genes can also be ordered on our PGxome Custom Panel. For ordering targeted known variants, please proceed to our Targeted Variants landing page. The great majority oftests are completed within 28 days. Detection rate of pathogenic variants in SLC4A1 and CA2 in a large cohort of patients with distal renal tubular acidosis (dRTA) is unknown in the literature because only a limited number of cases have been reported. In the original study that identified ATP6V1B1 pathogenic variants in autosomal recessive dRTA, Karet et al. studied 31 unrelated kindred (27 had family history of consanguineous marriage) and found ATP6V1B1 pathogenic variants in 19 (61%) cases (Karet et al. 1999). In another study of 26 patients with autosomal recessive dRTA, of which 23 were consanguineous, ATP6V1B1 pathogenic variants were found in 10 (38%) cases (Stover et al. 2002). In the original study that identified ATP6V0A4 pathogenic variants in autosomal recessive dRTA with normal hearing, Karet et al. studied 13 unrelated kindred (12 had family history of consanguineous marriage) and found ATP6V0A4 mutations in 9 (68%) cases (Karet et al. 1999). In another study of 26 patients with autosomal recessive dRTA, of which 23 were consanguineous, ATP6V0A4 pathogenic variants were found in 12 (46%) cases (Stover et al. 2002). Hereditary forms of distal renal tubular acidosis (dRTA) result from impaired acid excretion at intercalated cells in the collecting tubules and are characterized by hyperchloremic metabolic acidosis wi Continue reading >>

Distal Renal Tubular Acidosis Type 1

Distal Renal Tubular Acidosis Type 1

0 evaluations from distal renal tubular acidosis type 1 patients report major effectiveness of Venlafaxine for depressed mood (0%) 1 evaluation from a distal renal tubular acidosis type 1 patient reports moderate effectiveness of Venlafaxine for depressed mood (50%) 1 evaluation from a distal renal tubular acidosis type 1 patient reports slight effectiveness of Venlafaxine for depressed mood (50%) 0 evaluations from distal renal tubular acidosis type 1 patients report none effectiveness of Venlafaxine for depressed mood (0%) 0 evaluations from distal renal tubular acidosis type 1 patients report that they could not tell effectiveness of Venlafaxine for depressed mood (0%) 0 evaluations from distal renal tubular acidosis type 1 patients report severe overall side effects for Venlafaxine (0%) 0 evaluations from distal renal tubular acidosis type 1 patients report moderate overall side effects for Venlafaxine (0%) 2 evaluations from distal renal tubular acidosis type 1 patients report mild overall side effects for Venlafaxine (100%) 0 evaluations from distal renal tubular acidosis type 1 patients report no overall side effects for Venlafaxine (0%) 0 evaluations from distal renal tubular acidosis type 1 patients report major effectiveness of Gabapentin for pain (0%) 0 evaluations from distal renal tubular acidosis type 1 patients report moderate effectiveness of Gabapentin for pain (0%) 0 evaluations from distal renal tubular acidosis type 1 patients report slight effectiveness of Gabapentin for pain (0%) 1 evaluation from a distal renal tubular acidosis type 1 patient reports none effectiveness of Gabapentin for pain (100%) 0 evaluations from distal renal tubular acidosis type 1 patients report that they could not tell effectiveness of Gabapentin for pain (0%) 0 evaluatio Continue reading >>

Distal Renal Tubular Acidosis

Distal Renal Tubular Acidosis

Renal tubular acidosis - distal; Renal tubular acidosis type I; Type I RTA; RTA - distal; Classical RTA Distal renal tubular acidosis is a disease that occurs when the kidneys do not properly remove acids from the blood into the urine. As a result, too much acid remains in the blood (called acidosis ). The kidneys are responsible for removing wastes from the body, regulating electrolyte balance and blood pressure, and the stimulation of red blood cell production. This is the typical appearance of the blood vessels (vasculature) and urine flow pattern in the kidney. The blood vessels are shown in red and the urine flow pattern in yellow. When the body performs its normal functions, it produces acid. If this acid is not removed or neutralized, the blood becomes too acidic. This can lead to electrolyte imbalances in the blood. It can also cause problems with normal function of some cells. The kidneys help control the body's acid level by removing acid from the blood and excreting it into the urine. Distal renal tubular acidosis (Type I RTA) is caused by a defect in the kidney tubes that causes acid to build up in the blood. Type I RTA is caused by a variety of conditions, including: Amyloidosis , a buildup of abnormal protein, called amyloid, in the tissues and organs Fabry disease, an abnormal buildup in the body of a certain type of fatty substance Sickle cell disease , red blood cells that are normally shaped like a disk take on a sickle or crescent shape Sjgren syndrome , an autoimmune disorder in which the glands that produce tears and saliva are destroyed Systemic lupus erythematosus , an autoimmune disease in which the body's immune system mistakenly attacks healthy tissue Wilson disease , an inherited disorder in which there is too much copper in the body's tissue Continue reading >>

Distal Renal Tubular Acidosis

Distal Renal Tubular Acidosis

Also known as: Renal tubular acidosis - distal, Renal tubular acidosis type I, Type I RTA, RTA - distal or Classical RTA Distal renal tubular acidosis is a disease that occurs when the kidneys do not properly remove acids from the blood into the urine. As a result, too much acid remains in the blood (called acidosis ). When the body performs its normal functions, it produces acid. If this acid is not removed or neutralized, the blood becomes too acidic. This can lead to electrolyte imbalances in the blood. It can also cause problems with normal function of some cells. The kidneys help control the body's acid level by removing acid from the blood and excreting it into the urine. Distal renal tubular acidosis (Type I RTA) is caused by a defect in the kidney tubes that causes acid to build up in the blood. Type I RTA is caused by a variety of conditions, including: Amyloidosis , a buildup of abnormal protein, called amyloid, in the tissues and organs Fabry disease, an abnormal buildup in the body of a certain type of fatty substance Sickle cell disease , red blood cells that are normally shaped like a disk take on a sickle or crescent shape Sjgren syndrome , an autoimmune disorder in which the glands that produce tears and saliva are destroyed Systemic lupus erythematosus , an autoimmune disease in which the body's immune system mistakenly attacks healthy tissue Wilson disease , an inherited disorder in which there is too much copper in the body's tissues Use of certain medicines, such as amphotericin B, lithium, and analgesics Nephrocalcinosis (too much calcium deposited in the kidneys) The doctor will perform a physical exam and ask about your symptoms. The goal is to restore normal acid level and electrolyte balance in the body. This will help correct bone disorders an 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 >>

Hereditary Distal Renal Tubular Acidosis: New Understandings

Hereditary Distal Renal Tubular Acidosis: New Understandings

Hereditary Distal Renal Tubular Acidosis: New Understandings Daniel Batlle, Hrishikesh Ghanekar, Sheeja Jain, Amit Mitra Division of Nephrology/Hypertension, Northwestern University Medical School, 303 E. Chicago Avenue, Chicago, Illinois 60611-3008; e-mail: [emailprotected] Abstract The primary or hereditary form of distal renal tubular acidosis (dRTA), although rare, has received increased attention recently because of dramatic advances in the understanding of its genetic basis. The final regulation of renal acid excretion is effected by various acid/base transporters localized in specialized cells in the cortical collecting and outer medullary collecting tubules. Inherited defects in two of the key acid/base transporters involved in distal acidification, as well as mutations in the cytosolic carbonic anhydrase gene, can cause dRTA. The syndrome is inherited in both autosomal dominant and recessive patterns; patients with recessive dRTA present with either acute illness or growth failure at a young age, sometimes accompanied by deafness, whereas dominant dRTA is usually a milder disease and involves no hearing loss. The AE1 gene encodes two Cl/HCO3 exchangers that are expressed in the erythrocyte and in the acid-secreting intercalated cells of the kidney. AE1 contributes to urinary acidification by providing the major exit route for HCO3 across the basolateral membrane. Several mutations in the AE1 gene cosegregate with dominant dRTA. The modest degree of hypofunction exhibited in vitro by these mutations, however, does not explain the abnormal distal acidification phenotype. Other AE1 mutations have been linked to a recessive syndrome of dRTA and hemolytic anemia in which hypofunction can be discerned by in vitro studies. Several mutations in the carbonic anyhdrase 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 >>

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 >>

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