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Revision as of 16:51, 28 January 2021

Associate Editor(s)-in-Chief: Mydah Sajid, MD [1]

Microangiopathic hemolytic anemia must be differentiated from following diseases^[1]:


Disease	Findings
Pseudo-TTP (Vitamin B12 deficiency)	Patients have neurological symptoms like numbness, ataxic gait and tingling along with macrocytic anemia. There is a reduced level of reticulocytes, with elevated levels of Lactate dehydrogenase (i.e. greater than 5000 U/L), methylmalonate, and homocysteine.
Pregnancy induced fatty liver	Patients presents with right upper quadrant or epigastric abdominal pain, nausea and vomiting. On laboratory work-up, there is hypoglycemia along with deranged liver function tests. There is elevated levels of bilirubin, alanine aminotransferase, aspartate aminotransferase, reduced antithrombin III and coagulation factors level^[2].
Disseminated intravascular coagulation	Can occur in sepsis, and different malignancies like prostate cancer, Acute promyelocytic leukemia and Gastric cancer, there in increased consumption of fibrin. On laboratory work-up, there is reduced fibrinogen level, Auer rod in Acute promyelocytic leukemia and leukoerythroblastic picture, with nucleated [[red blood cell]s, poikilocytosis, left shift of white blood cells. In sepsis, there is elevation of procalcitonin along with positive blood culture and reduced levels of coagulation factors.
Endocarditis	Patients have multi-system involvement presenting with fever, sepsis, polyartharalgia, Janeway lesion, Osler’s node, and a new-onset or changed heart murmur. It is diagnosed clinically by Duke’s criteria. It is confirmed by blood culture and trans-esophageal echocardiography.
Evan's syndrome	Immune mediated thrombocytopenia and autoimmune hemolytic anemia. Coombs test positive. On peripheral blood smear, there are no schistocytes.
Antiphospholipid syndrome	Familial hypomagnesemia with hypercalciuria/nephrocalcinosis is an autosomal recessive disorder associated with hypercalciuria. The disease presents in childhood or adolescence with hypocalcemic symptoms. Renal insufficiency occurs as a result of nephrolithiasis and nephrocalcinosis. Familial hypomagnesemia with hypercalciuria/nephrocalcinosis is a result of a mutation in the claudin-16 gene (also known as paracellin-1). Claudin-16 is a tight junction protein that facilitates the passive, paracellular reabsorption of both magnesium and calcium in the thick ascending limb of the loop of Henle.^[3]^[4]^[5]^[6]^[7]
Cystic fibrosis	Patients with cystic fibrosis lose salt-rich sweat. Patients with moderate cystic fibrosis manifest with unexplained hypokalemia and metabolic alkalosis.^[8]^[9]^[10] In contrast to Bartter syndrome, spot urine chloride concentration is low in cystic fibrosis indicating chloride conservation in response to volume contraction.^[11]^[12]
Gullner syndrome - Familial hypokalemic alkalosis with proximal tubulopathy	Gullner syndrome presents with hypokalemic alkalosis, hyperreninemia, hyperaldosteronism, high urinary prostaglandin E2 excretion and normal blood pressure. Histologic examination of tissue obtained by biopsy from the kidneys showed intense staining of the proximal tubular cells, as well as extreme hypertrophy of the proximal tubular basement membranes. In contrast to Bartter syndrome, the juxtaglomerular apparatus were of normal appearance.^[13]
Activating mutations of the CaSR calcium-sensing receptor	Patients with activating mutation of the calcium-sensing receptor (CaSR) gene presents with potassium wasting, hypokalemia, and metabolic alkalosis, similar to Bartter syndrome.^[14]^[15] An activating (or gain-of-function) mutation of the calcium-sensing receptor (CaSR) gene impairs the calcium balance in the body and cause hypocalcemia. Activating mutation in the receptor increases the threshold for the receptor to detect the low calcium level. This causes the parathyroid hormone (PTH) to not release at serum calcium level that normally signals PTH release.^[16]^[17]^[18]
Hypomagnesemia	There are two major mechanisms by which hypomagnesemia can be induced such as gastrointestinal loss and renal loss. Hypomagnesemia is often associated with hypokalemia, hypocalcemia, and metabolic alkalosis.^[19] In contrast to Bartter syndrome, Hypomagnesemia is a common condition that occurs in up to 12 percent of hospitalized patients.^[20]
Congenital chloride diarrhea	Early diagnosis is a prerequisite for congenital chloride diarrhea in a newborn. It is a medical emergency that leads to severe dehydration and infant death.^[21] This disorder is due to a mutation in a gene that encodes an exchange protein, expressed in the ileum and colon, which works as a channel to absorbs chloride from the intestinal lumen and secretes bicarbonate. Mutation impairs the function of the chloride-bicarbonate channel and results in very high stool chloride concentrations (>100 mEq/L). In contrast to Bartter syndrome, the urinary chloride measurement is less than 20 mEq/L.^[22]
Hypochloremic alkalosis	Hypochloremic alkalosis is caused by an extreme lack or loss of chloride, such as from prolonged vomiting.^[23] In contrast to Bartter syndrome, the measurement of a spot urine chloride concentration is less than 25 mEq/l in hypochloremic alkalosis.^[24]
Hypokalemia	Hypokalemia can be induced by a gastrointestinal loss such as diarrhea and vomiting and urinary loss such as diuretic therapy. It can be induced transiently by entering into cells.^[25] Prolonged hypokalemia can lead to impaired ability of kidneys to concentrate urine, increased bicarbonate reabsorption. In contrast to Bartter syndrome, blood pressure is elevated in hypokalemia.^[26]

References

↑ Bommer M, Wölfle-Guter M, Bohl S, Kuchenbauer F (2018). "The Differential Diagnosis and Treatment of Thrombotic Microangiopathies". Dtsch Arztebl Int. 115 (19): 327–334. doi:10.3238/arztebl.2018.0327. PMC 5997890. PMID 29875054.
↑ Ko H, Yoshida EM (2006). "Acute fatty liver of pregnancy". Can J Gastroenterol. 20 (1): 25–30. doi:10.1155/2006/638131. PMC 2538964. PMID 16432556.
↑ Praga M, Vara J, González-Parra E, Andrés A, Alamo C, Araque A; et al. (1995). "Familial hypomagnesemia with hypercalciuria and nephrocalcinosis". Kidney Int. 47 (5): 1419–25. doi:10.1038/ki.1995.199. PMID 7637271.
↑ Nicholson JC, Jones CL, Powell HR, Walker RG, McCredie DA (1995). "Familial hypomagnesaemia--hypercalciuria leading to end-stage renal failure". Pediatr Nephrol. 9 (1): 74–6. doi:10.1007/BF00858976. PMID 7742227.
↑ Benigno V, Canonica CS, Bettinelli A, von Vigier RO, Truttmann AC, Bianchetti MG (2000). "Hypomagnesaemia-hypercalciuria-nephrocalcinosis: a report of nine cases and a review". Nephrol Dial Transplant. 15 (5): 605–10. doi:10.1093/ndt/15.5.605. PMID 10809799.
↑ Müller D, Kausalya PJ, Bockenhauer D, Thumfart J, Meij IC, Dillon MJ; et al. (2006). "Unusual clinical presentation and possible rescue of a novel claudin-16 mutation". J Clin Endocrinol Metab. 91 (8): 3076–9. doi:10.1210/jc.2006-0200. PMID 16705067.
↑ Konrad M, Hou J, Weber S, Dötsch J, Kari JA, Seeman T; et al. (2008). "CLDN16 genotype predicts renal decline in familial hypomagnesemia with hypercalciuria and nephrocalcinosis". J Am Soc Nephrol. 19 (1): 171–81. doi:10.1681/ASN.2007060709. PMC 2391030. PMID 18003771.
↑ Kose M, Pekcan S, Ozcelik U, Cobanoglu N, Yalcin E, Dogru D; et al. (2008). "An epidemic of pseudo-Bartter syndrome in cystic fibrosis patients". Eur J Pediatr. 167 (1): 115–6. doi:10.1007/s00431-007-0413-3. PMID 17323076.
↑ Kennedy JD, Dinwiddie R, Daman-Willems C, Dillon MJ, Matthew DJ (1990). "Pseudo-Bartter's syndrome in cystic fibrosis". Arch Dis Child. 65 (7): 786–7. doi:10.1136/adc.65.7.786. PMC 1792454. PMID 2386386.
↑ Bates CM, Baum M, Quigley R (1997). "Cystic fibrosis presenting with hypokalemia and metabolic alkalosis in a previously healthy adolescent". J Am Soc Nephrol. 8 (2): 352–5. PMID 9048354.
↑ Davé S, Honney S, Raymond J, Flume PA (2005). "An unusual presentation of cystic fibrosis in an adult". Am J Kidney Dis. 45 (3): e41–4. doi:10.1053/j.ajkd.2004.11.009. PMID 15754262.
↑ Leoni GB, Pitzalis S, Podda R, Zanda M, Silvetti M, Caocci L; et al. (1995). "A specific cystic fibrosis mutation (T3381) associated with the phenotype of isolated hypotonic dehydration". J Pediatr. 127 (2): 281–3. doi:10.1016/s0022-3476(95)70310-1. PMID 7543567.
↑ Güllner HG, Bartter FC, Gill JR, Dickman PS, Wilson CB, Tiwari JL (1983). "A sibship with hypokalemic alkalosis and renal proximal tubulopathy". Arch Intern Med. 143 (8): 1534–40. doi:10.1001/archinte.1983.00350080040011. PMID 6347111.
↑ Watanabe S, Fukumoto S, Chang H, Takeuchi Y, Hasegawa Y, Okazaki R; et al. (2002). "Association between activating mutations of calcium-sensing receptor and Bartter's syndrome". Lancet. 360 (9334): 692–4. doi:10.1016/S0140-6736(02)09842-2. PMID 12241879.
↑ Konrad M, Weber S (2003). "Recent advances in molecular genetics of hereditary magnesium-losing disorders". J Am Soc Nephrol. 14 (1): 249–60. doi:10.1097/01.asn.0000049161.60740.ce. PMID 12506158.
↑ Brown EM (2007). "Clinical lessons from the calcium-sensing receptor". Nat Clin Pract Endocrinol Metab. 3 (2): 122–33. doi:10.1038/ncpendmet0388. PMID 17237839.
↑ Pollak MR, Brown EM, Estep HL, McLaine PN, Kifor O, Park J; et al. (1994). "Autosomal dominant hypocalcaemia caused by a Ca(2+)-sensing receptor gene mutation". Nat Genet. 8 (3): 303–7. doi:10.1038/ng1194-303. PMID 7874174.
↑ D'Souza-Li L, Yang B, Canaff L, Bai M, Hanley DA, Bastepe M; et al. (2002). "Identification and functional characterization of novel calcium-sensing receptor mutations in familial hypocalciuric hypercalcemia and autosomal dominant hypocalcemia". J Clin Endocrinol Metab. 87 (3): 1309–18. doi:10.1210/jcem.87.3.8280. PMID 11889203.
↑ Tong GM, Rude RK (2005). "Magnesium deficiency in critical illness". J Intensive Care Med. 20 (1): 3–17. doi:10.1177/0885066604271539. PMID 15665255.
↑ Wong ET, Rude RK, Singer FR, Shaw ST (1983). "A high prevalence of [[hypomagnesemia]] and [[hypermagnesemia]] in hospitalized patients". Am J Clin Pathol. 79 (3): 348–52. doi:10.1093/ajcp/79.3.348. PMID 6829504. URL–wikilink conflict (help)
↑ Wedenoja S, Höglund P, Holmberg C (2010). "Review article: the clinical management of congenital chloride diarrhoea". Aliment Pharmacol Ther. 31 (4): 477–85. doi:10.1111/j.1365-2036.2009.04197.x. PMID 19912155.
↑ EVANSON JM, STANBURY SW (1965). "CONGENITAL CHLORIDORRHOEA OR SO-CALLED CONGENITAL ALKALOSIS WITH DIARRHOEA". Gut. 6: 29–38. doi:10.1136/gut.6.1.29. PMC 1552247. PMID 14259421.
↑ "Alkalosis: MedlinePlus Medical Encyclopedia".
↑ Veldhuis JD, Bardin CW, Demers LM (1979). "Metabolic mimicry of Bartter's syndrome by covert vomiting: utility of urinary chloride determinations". Am J Med. 66 (2): 361–3. doi:10.1016/0002-9343(79)90566-7. PMID 425977.
↑ Gennari FJ (1998). "Hypokalemia". N Engl J Med. 339 (7): 451–8. doi:10.1056/NEJM199808133390707. PMID 9700180.
↑ Kim GH, Han JS (2002). "Therapeutic approach to hypokalemia". Nephron. 92 Suppl 1: 28–32. doi:10.1159/000065374. PMID 12401935.

Template:WH Template:WS

[pmid29875054-1] Bommer M, Wölfle-Guter M, Bohl S, Kuchenbauer F (2018). "The Differential Diagnosis and Treatment of Thrombotic Microangiopathies". Dtsch Arztebl Int. 115 (19): 327–334. doi:10.3238/arztebl.2018.0327. PMC 5997890. PMID 29875054.

[pmid16432556-2] Ko H, Yoshida EM (2006). "Acute fatty liver of pregnancy". Can J Gastroenterol. 20 (1): 25–30. doi:10.1155/2006/638131. PMC 2538964. PMID 16432556.

[pmid7637271-3] Praga M, Vara J, González-Parra E, Andrés A, Alamo C, Araque A; et al. (1995). "Familial hypomagnesemia with hypercalciuria and nephrocalcinosis". Kidney Int. 47 (5): 1419–25. doi:10.1038/ki.1995.199. PMID 7637271.

[pmid7742227-4] Nicholson JC, Jones CL, Powell HR, Walker RG, McCredie DA (1995). "Familial hypomagnesaemia--hypercalciuria leading to end-stage renal failure". Pediatr Nephrol. 9 (1): 74–6. doi:10.1007/BF00858976. PMID 7742227.

[pmid10809799-5] Benigno V, Canonica CS, Bettinelli A, von Vigier RO, Truttmann AC, Bianchetti MG (2000). "Hypomagnesaemia-hypercalciuria-nephrocalcinosis: a report of nine cases and a review". Nephrol Dial Transplant. 15 (5): 605–10. doi:10.1093/ndt/15.5.605. PMID 10809799.

[pmid16705067-6] Müller D, Kausalya PJ, Bockenhauer D, Thumfart J, Meij IC, Dillon MJ; et al. (2006). "Unusual clinical presentation and possible rescue of a novel claudin-16 mutation". J Clin Endocrinol Metab. 91 (8): 3076–9. doi:10.1210/jc.2006-0200. PMID 16705067.

[pmid18003771-7] Konrad M, Hou J, Weber S, Dötsch J, Kari JA, Seeman T; et al. (2008). "CLDN16 genotype predicts renal decline in familial hypomagnesemia with hypercalciuria and nephrocalcinosis". J Am Soc Nephrol. 19 (1): 171–81. doi:10.1681/ASN.2007060709. PMC 2391030. PMID 18003771.

[pmid17323076-8] Kose M, Pekcan S, Ozcelik U, Cobanoglu N, Yalcin E, Dogru D; et al. (2008). "An epidemic of pseudo-Bartter syndrome in cystic fibrosis patients". Eur J Pediatr. 167 (1): 115–6. doi:10.1007/s00431-007-0413-3. PMID 17323076.

[pmid2386386-9] Kennedy JD, Dinwiddie R, Daman-Willems C, Dillon MJ, Matthew DJ (1990). "Pseudo-Bartter's syndrome in cystic fibrosis". Arch Dis Child. 65 (7): 786–7. doi:10.1136/adc.65.7.786. PMC 1792454. PMID 2386386.

[pmid9048354-10] Bates CM, Baum M, Quigley R (1997). "Cystic fibrosis presenting with hypokalemia and metabolic alkalosis in a previously healthy adolescent". J Am Soc Nephrol. 8 (2): 352–5. PMID 9048354.

[pmid15754262-11] Davé S, Honney S, Raymond J, Flume PA (2005). "An unusual presentation of cystic fibrosis in an adult". Am J Kidney Dis. 45 (3): e41–4. doi:10.1053/j.ajkd.2004.11.009. PMID 15754262.

[pmid7543567-12] Leoni GB, Pitzalis S, Podda R, Zanda M, Silvetti M, Caocci L; et al. (1995). "A specific cystic fibrosis mutation (T3381) associated with the phenotype of isolated hypotonic dehydration". J Pediatr. 127 (2): 281–3. doi:10.1016/s0022-3476(95)70310-1. PMID 7543567.

[pmid6347111-13] Güllner HG, Bartter FC, Gill JR, Dickman PS, Wilson CB, Tiwari JL (1983). "A sibship with hypokalemic alkalosis and renal proximal tubulopathy". Arch Intern Med. 143 (8): 1534–40. doi:10.1001/archinte.1983.00350080040011. PMID 6347111.

[pmid12241879-14] Watanabe S, Fukumoto S, Chang H, Takeuchi Y, Hasegawa Y, Okazaki R; et al. (2002). "Association between activating mutations of calcium-sensing receptor and Bartter's syndrome". Lancet. 360 (9334): 692–4. doi:10.1016/S0140-6736(02)09842-2. PMID 12241879.

[pmid12506158-15] Konrad M, Weber S (2003). "Recent advances in molecular genetics of hereditary magnesium-losing disorders". J Am Soc Nephrol. 14 (1): 249–60. doi:10.1097/01.asn.0000049161.60740.ce. PMID 12506158.

[pmid17237839-16] Brown EM (2007). "Clinical lessons from the calcium-sensing receptor". Nat Clin Pract Endocrinol Metab. 3 (2): 122–33. doi:10.1038/ncpendmet0388. PMID 17237839.

[pmid7874174-17] Pollak MR, Brown EM, Estep HL, McLaine PN, Kifor O, Park J; et al. (1994). "Autosomal dominant hypocalcaemia caused by a Ca(2+)-sensing receptor gene mutation". Nat Genet. 8 (3): 303–7. doi:10.1038/ng1194-303. PMID 7874174.

[pmid11889203-18] D'Souza-Li L, Yang B, Canaff L, Bai M, Hanley DA, Bastepe M; et al. (2002). "Identification and functional characterization of novel calcium-sensing receptor mutations in familial hypocalciuric hypercalcemia and autosomal dominant hypocalcemia". J Clin Endocrinol Metab. 87 (3): 1309–18. doi:10.1210/jcem.87.3.8280. PMID 11889203.

[pmid15665255-19] Tong GM, Rude RK (2005). "Magnesium deficiency in critical illness". J Intensive Care Med. 20 (1): 3–17. doi:10.1177/0885066604271539. PMID 15665255.

[pmid6829504-20] Wong ET, Rude RK, Singer FR, Shaw ST (1983). "A high prevalence of [[hypomagnesemia]] and [[hypermagnesemia]] in hospitalized patients". Am J Clin Pathol. 79 (3): 348–52. doi:10.1093/ajcp/79.3.348. PMID 6829504. URL–wikilink conflict (help)

[pmid19912155-21] Wedenoja S, Höglund P, Holmberg C (2010). "Review article: the clinical management of congenital chloride diarrhoea". Aliment Pharmacol Ther. 31 (4): 477–85. doi:10.1111/j.1365-2036.2009.04197.x. PMID 19912155.

[pmid14259421-22] EVANSON JM, STANBURY SW (1965). "CONGENITAL CHLORIDORRHOEA OR SO-CALLED CONGENITAL ALKALOSIS WITH DIARRHOEA". Gut. 6: 29–38. doi:10.1136/gut.6.1.29. PMC 1552247. PMID 14259421.

[urlAlkalosis:_MedlinePlus_Medical_Encyclopedia-23] "Alkalosis: MedlinePlus Medical Encyclopedia".

[pmid425977-24] Veldhuis JD, Bardin CW, Demers LM (1979). "Metabolic mimicry of Bartter's syndrome by covert vomiting: utility of urinary chloride determinations". Am J Med. 66 (2): 361–3. doi:10.1016/0002-9343(79)90566-7. PMID 425977.

[pmid9700180-25] Gennari FJ (1998). "Hypokalemia". N Engl J Med. 339 (7): 451–8. doi:10.1056/NEJM199808133390707. PMID 9700180.

[pmid12401935-26] Kim GH, Han JS (2002). "Therapeutic approach to hypokalemia". Nephron. 92 Suppl 1: 28–32. doi:10.1159/000065374. PMID 12401935.

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@@ Line 12: / Line 12: @@
 | style="padding: 5px 5px; background: #F5F5F5;" |
 * [[Patient]]s have [[neurological]] symptoms like [[numbness]], [[ataxic]] gait and [[tingling]] along with [[macrocytic anemia]].
-* There is reduced level of [[reticulocyte]]s, with elevated levels of [[LDH|Lactate dehydrogenase]] (i.e. greater than 5000 U/L), methylmalonate and homocysteine.
+* There is a reduced level of [[reticulocyte]]s, with elevated levels of [[LDH|Lactate dehydrogenase]] (i.e. greater than 5000 U/L), methylmalonate, and homocysteine.
 |-
 | style="padding: 5px 5px; background: #DCDCDC;" | '''[[Pregnancy]] induced [[fatty liver]]'''
@@ Line 23: / Line 23: @@
 | style="padding: 5px 5px; background: #DCDCDC;" | '''[[DIC|Disseminated intravascular coagulation]]'''
 | style="padding: 5px 5px; background: #F5F5F5;" |
-* In different malignancies like [[prostate cancer]], [[Acute promyelocytic leukemia]] and [[Gastric cancer]], there in increased consumption of [[fibrin]].
+* Can occur in [[sepsis]], and different malignancies like [[prostate cancer]], [[Acute promyelocytic leukemia]] and [[Gastric cancer]], there in increased consumption of [[fibrin]].
 * On laboratory work-up, there is reduced [[fibrinogen]] level, [[Auer rod]] in [[Acute promyelocytic leukemia]] and leukoerythroblastic picture, with nucleated [[red blood cell]s, [[poikilocytosis]], left shift of [[white blood cells]].
+* In [[sepsis]], there is elevation of [[procalcitonin]] along with positive [[blood culture]] and reduced levels of [[coagulation factors]].
 |-
 | style="padding: 5px 5px; background: #DCDCDC;" |'''[[Endocarditis]]'''
@@ Line 32: / Line 33: @@
 * It is confirmed by [[blood]] [[culture]] and trans-esophageal [[echocardiography]].
 |-
-| style="padding: 5px 5px; background: #DCDCDC;" | '''Hyperprostaglandin E syndrome'''
+| style="padding: 5px 5px; background: #DCDCDC;" | '''Evan's syndrome'''
 | style="padding: 5px 5px; background: #F5F5F5;" |
-*Hyperprostaglandin E syndrome(HPS) occurs during [[pregnancy]] before a birth. It is an antenatal variant of [[Bartter syndrome]] characterized by [[polyhydramnios]] and [[preterm delivery]]. In the [[postnatal period]], it is characterized by [[salt-wasting]], [[hypercalciuria]], and [[nephrocalcinosis]].<ref name="pmid19014056">{{cite journal| author=Cetinkaya M, Köksal N, Ozkan H, Dönmez O, Sağlam H, Kiriştioğlu I| title=Hyperprostaglandin E syndrome: use of indomethacin and steroid, and death due to necrotizing enterocolitis and sepsis. | journal=Turk J Pediatr | year= 2008 | volume= 50 | issue= 4 | pages= 386-90 | pmid=19014056 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19014056  }} </ref>
+* [[Immune]] mediated [[thrombocytopenia]] and [[autoimmune hemolytic anemia]].
+* [[Coombs test]] positive. On [[peripheral blood smear]], there are no [[schistocytes]].
 |-
-| style="padding: 5px 5px; background: #DCDCDC;" | '''Familial hypomagnesemia with hypercalciuria/nephrocalcinosis'''
+| style="padding: 5px 5px; background: #DCDCDC;" | '''Antiphospholipid syndrome'''
 | style="padding: 5px 5px; background: #F5F5F5;" |
 *Familial [[hypomagnesemia]] with [[hypercalciuria]]/[[nephrocalcinosis]] is an [[autosomal recessive]] disorder associated with [[hypercalciuria]]. The disease presents in childhood or adolescence with [[hypocalcemia|hypocalcemic]] symptoms.
@@ Line 53: / Line 55: @@
 *Histologic examination of tissue obtained by biopsy from the kidneys showed intense staining of the [[tubular cells|proximal tubular cells]], as well as extreme hypertrophy of the [[basement membrane|proximal tubular basement membranes]].
 *In contrast to [[Bartter syndrome]], the [[juxtaglomerular apparatus]] were of normal appearance.<ref name="pmid6347111">{{cite journal| author=Güllner HG, Bartter FC, Gill JR, Dickman PS, Wilson CB, Tiwari JL| title=A sibship with hypokalemic alkalosis and renal proximal tubulopathy. | journal=Arch Intern Med | year= 1983 | volume= 143 | issue= 8 | pages= 1534-40 | pmid=6347111 | doi=10.1001/archinte.1983.00350080040011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=6347111  }} </ref>
-|-
-| style="padding: 5px 5px; background: #DCDCDC;" | '''[[Mineralocorticoid excess]]'''
-| style="padding: 5px 5px; background: #F5F5F5;" |
-*[[Mineralocorticoid]] excess is presented with [[low birth weight]], [[failure to thrive]], [[hypercalciuria]] and [[nephrocalcinosis]] from an unknown mechanism, and [[renal failure]].
-*In contrast to [[Bartter syndrome]], severe [[hypertension]] in early childhood with extensive target organ damage occurs in [[mineralocorticoid excess]].<ref name="pmid17035606">{{cite journal| author=Morineau G, Sulmont V, Salomon R, Fiquet-Kempf B, Jeunemaître X, Nicod J | display-authors=etal| title=Apparent mineralocorticoid excess: report of six new cases and extensive personal experience. | journal=J Am Soc Nephrol | year= 2006 | volume= 17 | issue= 11 | pages= 3176-84 | pmid=17035606 | doi=10.1681/ASN.2006060570 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17035606  }} </ref>
-*In contrast to [[Bartter syndrome]], [[mineralocorticoid excess]] is characterized by low plasma [[renin]] and [[aldosterone]].<ref name="pmid9661590">{{cite journal| author=Dave-Sharma S, Wilson RC, Harbison MD, Newfield R, Azar MR, Krozowski ZS | display-authors=etal| title=Examination of genotype and phenotype relationships in 14 patients with apparent mineralocorticoid excess. | journal=J Clin Endocrinol Metab | year= 1998 | volume= 83 | issue= 7 | pages= 2244-54 | pmid=9661590 | doi=10.1210/jcem.83.7.4986 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9661590  }} </ref><ref name="pmid20733335">{{cite journal| author=Bockenhauer D, van't Hoff W, Dattani M, Lehnhardt A, Subtirelu M, Hildebrandt F | display-authors=etal| title=Secondary nephrogenic diabetes insipidus as a complication of inherited renal diseases. | journal=Nephron Physiol | year= 2010 | volume= 116 | issue= 4 | pages= p23-9 | pmid=20733335 | doi=10.1159/000320117 | pmc=3896046 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20733335  }} </ref>
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 | style="padding: 5px 5px; background: #DCDCDC;" | '''Activating mutations of the CaSR calcium-sensing receptor'''

Microangiopathic hemolytic anemia differential diagnosis: Difference between revisions

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