8.5 Renal Tubular Acidosis
Renal Tubular Acidosis (RTA) is a syndrome due to either a defect in proximal tubule bicarbonate reabsorption, or a defect in distal tubule hydrogen ion secretion, or both. This results in a hyperchloraemic metabolic acidosis with normal to moderately decreased GFR. Anion gap is normal. A typical situation where RTA would be suspected is if urine pH is greater than 7.0 despite the presence of a metabolic acidosis. In contrast, the acidosis that occurs with acute, chronic, or acute on chronic renal failure is a high anion gap metabolic acidosis. As a general overview to help understand why renal disease can give different types of acidosis consider the following:Acidosis due to renal disease is considered in 2 categories depending on whether the predominant site of renal damage is in the glomeruli or in the tubules. Renal tubular acidosis is a form of hyperchloraemic metabolic acidosis which occurs when the renal damage primarily affects tubular function without much effect on glomerular function. The result is a decrease in H+ excretion which is greater than can be explained by any change in GFR. In contrast, if glomerular function (ie GFR) is significantly depressed (hence 'renal failure'), the retention of fixed acids results in a high anion gap acidosis. Predominantly tubular damage ---> Normal anion gap acidosis (Renal tubular acidosis - RTA) Predominantly glomerular damage ---> High anion gap acidosis Three main clinical categories or 'types' of renal tubular acidosis (RTA) are now recognised but the number of possible causes is large. The mechanism causing the defect in ability to acidify the urine and excrete acid is different in the three types. 1,2 8.5.2 Distal (Type 1) Renal Tubular Acidosis This is also referred to as classic RTA or distal RTA. The problem h Continue reading >>
Genetic Causes And Mechanisms Of Distal Renal Tubular Acidosis
Genetic causes and mechanisms of distal renal tubular acidosis Northwestern University Feinberg School of Medicine Correspondence and offprint requests to: Daniel Batlle; E-mail: [email protected] Search for other works by this author on: Northwestern University Feinberg School of Medicine Nephrology Dialysis Transplantation, Volume 27, Issue 10, 1 October 2012, Pages 36913704, Daniel Batlle, Syed K. Haque; Genetic causes and mechanisms of distal renal tubular acidosis, Nephrology Dialysis Transplantation, Volume 27, Issue 10, 1 October 2012, Pages 36913704, The primary or hereditary forms of distal renal tubular acidosis (dRTA) have received increased attention because of advances in the understanding of the molecular mechanism, whereby mutations in the main proteins involved in acidbase transport result in impaired acid excretion. Dysfunction of intercalated cells in the collecting tubules accounts for all the known genetic causes of dRTA. These cells secrete protons into the tubular lumen through H+-ATPases functionally coupled to the basolateral anion exchanger 1 (AE1). The substrate for both transporters is provided by the catalytic activity of the cytosolic carbonic anhydrase II (CA II), an enzyme which is also present in the proximal tubular cells and osteoclasts. Mutations in ATP6V1B1, encoding the B-subtype unit of the apical H(+) ATPase, and ATP6V0A4, encoding the a-subtype unit, lead to the loss of function of the apical H(+) ATPase and are usually responsible for patients with autosomal recessive dRTA often associated with early or late sensorineural deafness. Mutations in the gene encoding the cytosolic CA II are associated with the autosomal recessive syndrome of osteopetrosis, mixed distal and proximal RTA and cerebral calcification. Mutations in Continue reading >>
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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 >>
Proximal Renal Tubular Acidosis
URL of this page: //medlineplus.gov/ency/article/000497.htm Proximal renal tubular acidosis is a disease that occurs when the kidneys don't 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 will become 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. Acidic substances in the body are neutralized by alkaline substances, mainly bicarbonate. Proximal renal tubular acidosis (Type II RTA) occurs when bicarbonate is not properly reabsorbed by the kidney's filtering system. Type II RTA is less common than Type I RTA. Type I is also called distal renal tubular acidosis . Type II most often occurs during infancy and may go away by itself. Cystinosis (body is unable to break down the substance cysteine) Drugs such as ifosfamide (a chemotherapy drug), certain antibiotics that are no longer used much (tetracycline), or acetazolamide Fanconi syndrome , a disorder of the kidney tubes in which certain substances normally absorbed into the bloodstream by the kidneys are released into the urine instead Inherited fructose intolerance , a disorder in which there is a lack of the protein needed to break down the fruit sugar fructose Multiple myeloma , a type of blood cancer Primary hyperparathyroidism , a disorder in which the parathyroid glands in the neck produce too much parathyroid hormone Sjgren syndrome , an autoimmune disorder in which the glands that produce tears and saliva are destroyed Wilson disease , an Continue reading >>
Renal Tubular Acidosis (rta): Types, Causes, Symptoms, Diagnosis & Treatment
Renal Tubular Acidosis or RTA is a kidney disease in which the kidneys are unable to maintain the acid-base balance in the body. The condition causes increased acidic contents in the blood and decreases excretion of acid molecules in urine. In this article, we will read about the different causes, symptoms, and treatments for Renal Tubular Acidosis. Renal Tubular Acidosis (RTA) causes accumulation of acidic content in the body Increased accumulation of acid in the blood is caused by kidney failure resulting in decreased excretion of acid in urine. Acid content in the blood increases because of following reason- Kidney is unable to retain alkaline molecules or bicarbonates. Kidney retains and is unable to discharge hydrogen molecules or acid content in the urine. Renal tubular acidosis causes metabolic acidosis. Renal tubular acidosis reduces blood pH resulting in academia. This condition is also called Distal Renal Tubular Acidosis. This is one of the most common forms of Renal Tubular Acidosis. The disease is caused by reduced hydrogen (acid) molecules excretion in distal tubule and increased excretion of HCO3 (alkaline) molecule. The H+ molecule is reabsorbed as acid molecule causing decreased blood pH or acidic pH resulting in metabolic acidosis. Type 1 Renal Tubular Acidosis is associated with renal stone.1 Plasma HCO3 level is less the 15 mEq/L (normal level over 23 mEq/L). Plasma K level is low resulting in hypokalemia.1 This condition is associated with high levels of calcium in the blood Renal tubular acidosis is often observed in patients suffering with sickle cell disease, lupus and Sjogren syndrome. This disease is also known as Proximal Renal Tubular Acidosis. The defect is in close proximity to the origin of the tubule. Disease is caused by defects in proxi Continue reading >>
Orphanet: Proximal 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 Proximal renal tubular acidosis (pRTA) is a tubular kidney disease characterized by impaired ability of the proximal tubule to reabsorb bicarbonate from the glomerular filtrate leading to hyperchloremic metabolic acidosis. Inheritance: Autosomal dominantorAutosomal recessiveorNot applicable Prevalence is unknown but isolated hereditary pRTA is very rare. Drug-induced pRTA occurs relatively frequently. The onset of hereditary pRTA varies from infancy to adulthood, manifesting initially with very alkaline urine due to bicarbonate wastage. Autosomal recessive pRTA (AR pRTA; see this term) is associated with severe growth retardation leading to short stature, intellectual disability and ocular abnormalities such as band keratopathy, cataracts, and glaucoma. Growth retardation and reduced bone density, due to metabolic acidosis, are seen in autosomal dominant pRTA (AD pRTA; see this term). Hypokalemia may be present in some cases of pRTA and can occasionally cause symptoms of hypokalemic periodic paralysis (see this term). Rickets and osteomalacia are common due to vitamin D deficiency and phosphate wasting. In cases where pRTA is associated with primary Fanconi syndrome (see this term), glycosuria, aminoaciduria, phosphaturia, uric acid wastage and tubular proteinuria can occur. Isolated pRTA can be acquired or is inherited either recessively (in most cases) or dominantly. AR pRTA is due to a mutation in the SLC4A4 gene (4q13.3) that encodes the electrogenic sodium bicarbonate cotransporte Continue reading >>
Vetfolio
This article discusses the pathophysiology, causes, diagnosis, treatment, and prognosis of renal tubular acidosis (RTA) in veterinary patients. RTA is classified as a non-anion-gap metabolic acidosis in the presence of a normal glomerular filtration rate. Proximal RTA occurs because of a deficiency in bicarbonate resorption in the proximal tubule, whereas distal RTA occurs because of decreased production of bicarbonate in the distal tubule. RTA can be transient or permanent and can occur secondary to other diseases. Therapy includes bicarbonate supplementation with careful acid-base and electrolyte monitoring and treatment of underlying causes. There are few published discussions of renal tubular acidosis (RTA) in the veterinary literature despite the abundance of reports of such disorders in humans. Although it is possible that the incidence of such conditions in small animals is less than that in humans, it is also plausible that tubular disorders are overlooked in veterinary patients (Table 1). RTA typically causes metabolic acidosis with both a normal anion gap and normal glomerular filtration rate (GFR). In contrast, renal failure is often associated with an increased anion gap due to the presence of phosphates, sulfates, and organic anions as well as a reduced GFR. Traditionally, RTA has been classified into four types in human medicine: type 1 (i.e., distal tubular acidosis), type 2 (i.e., proximal tubular acidosis), type 3 (i.e., an ill-defined combination of proximal and distal tubular acidosis), and type 4 (i.e., hyperkalemic RTA). Type 3 RTA is an obsolete term because it is no longer considered a distinct form of RTA. Type 4 RTA is associated with hyperkalemia and decreased renin and aldosterone concentrations. In humans, this is most commonly recognized in Continue reading >>
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
Significant bilateral nephrocalcinosis (calcification of the kidneys) on a frontal X-ray (radiopacities (white) in the right upper and left upper quadrant of the image), as seen in distal renal tubular acidosis. Renal tubular acidosis (RTA) is a medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately acidify the urine . [1] In renal physiology , when blood is filtered by the kidney, the filtrate passes through the tubules of the nephron , allowing for exchange of salts , acid equivalents, and other solutes before it drains into the bladder as urine . The metabolic acidosis that results from RTA may be caused either by failure to reabsorb sufficient bicarbonate ions (which are alkaline ) from the filtrate in the early portion of the nephron (the proximal tubule ) or by insufficient secretion of hydrogen ions (which are acidic) into the latter portions of the nephron (the distal tubule ). Although a metabolic acidosis also occurs in those with renal insufficiency , the term RTA is reserved for individuals with poor urinary acidification in otherwise well-functioning kidneys. Several different types of RTA exist, which all have different syndromes and different causes. The word acidosis refers to the tendency for RTA to cause an excess of acid , which lowers the blood's pH . When the blood pH is below normal (7.35), this is called acidemia . The metabolic acidosis caused by RTA is a normal anion gap acidosis . Failure of proximal tubular cells to reabsorb H C O 3 Deficiency of aldosterone , or a resistance to its effects, ( hypoaldosteronism or pseudohypoaldosteronism ) Main article: Distal renal tubular acidosis Radiograph of a child with rickets , a complication of both distal and proximal RTA. Distal RTA (dRT Continue reading >>
Renal Tubular Disease
Zhuo JL, Li XC ; Proximal nephron. Compr Physiol. 2013 Jul3(3):1079-123. doi: 10.1002/cphy.c110061. Fiseha T, Gebreweld A ; Urinary Markers of Tubular Injury in HIV-Infected Patients. Biochem Res Int. 20162016:1501785. doi: 10.1155/2016/1501785. Epub 2016 Jul 17. Bagga A et al ; Approach to Renal Tubular Disorders Indian Journal of Pediatrics Volume 72-September, 2005. Distal renal tubular acidosis ; Orphanet, 2014 Rehman HU ; A woman with generalised weakness, hypokalaemia, and metabolic acidosis. BMJ. 2012 Apr 12344:e2545. doi: 10.1136/bmj.e2545. Both T, Zietse R, Hoorn EJ, et al ; Everything you need to know about distal renal tubular acidosis in autoimmune disease. Rheumatol Int. 2014 Aug34(8):1037-45. doi: 10.1007/s00296-014-2993-3. Epub 2014 Mar 29. Renal tubular acidosis ; BMJ Best Practice, 2016. Walsh SB, Unwin RJ ; Renal tubular disorders. Clin Med October 1, 2012 vol. 12 no. 5 476-479. Goswami RP, Mondal S, Karmakar PS, et al ; Type 3 renal tubular acidosis. Indian J Nephrol. 2012 Nov22(6):466-8. doi: 10.4103/0971-4065.106058. Haas CS, Pohlenz I, Lindner U, et al ; Renal tubular acidosis type IV in hyperkalaemic patients--a fairy tale or reality? Clin Endocrinol (Oxf). 2013 May78(5):706-11. doi: 10.1111/j.1365-2265.2012.04446.x. Karunarathne S, Udayakumara Y, Govindapala D, et al ; Type IV renal tubular acidosis following resolution of acute kidney injury and disseminated intravascular coagulation due to hump-nosed viper bite. Indian J Nephrol. 2013 Jul23(4):294-6. doi: 10.4103/0971-4065.114476. Prasad N, Bhadauria D ; Renal phosphate handling: Physiology. Indian J Endocrinol Metab. 2013 Jul17(4):620-7. doi: 10.4103/2230-8210.113752. Moutzouri E, Liberopoulos EN, Elisaf M ; Life-threatening hypophosphataemia in a cirrhotic patient with jaundice. Arch Med Sci Continue reading >>
Renal Tubular Acidosis
Renal tubular acidosis (RTA) refers to the non-anion gap metabolic acidosis which develops due to derangement of usual metabolic processes in the kidneys. The kidneys have a critical role in maintaining stable physiologic pH and they do so through several mechanisms throughout the nephron. Proximally, filtered bicarbonate is resorbed and distally acid is excreted then buffered in the urine. If the kidneys lose the ability to carry out these functions, renal tubular acidosis results. The three major forms of renal tubular acidosis are differentiated by the specific type and location of the mechanistic defect. An understanding of the basic physiology of the handling of acid by the kidney allows one to use clinical and laboratory clues to diagnose the type of RTA. The three key renal mechanisms to handle acid are listed below with the form of RTA associated with defects at that site. Reclaiming filtered bicarbonate in the proximal tubule - proximal (type 2) renal tubular acidosis The reclamation of bicarbonate is accompanied by excretion of a proton (H+) and occurs primarily in the proximal tubule (90% of filtered bicarbonate). A decrease in proximal tubular bicarbonate resorptive capacity results in proximal (type 2) RTA. During the development of proximal RTA, bicarbonate is excreted into the urine because the filtered concentration exceeds the resorptive threshold of the proximal tubule, raising the urine pH. However, due to urinary loss, the subsequent serum and filtered bicarbonate concentrations decrease below the resorptive threshold such that filtered bicarbonate is then resorbed normally. Therefore the bicarbonaturia is self-limited and the serum bicarbonate concentration usually stabilizes between 14 and 20 meq/L. The urine pH is only transiently elevated during Continue reading >>
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 >>
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 >>
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 >>
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 >>
