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Article ; Online: Comments on Trachtman et al.: Recurrent focal segmental glomerulosclerosis after kidney transplantation.

Straatmann, Caroline / Vehaskari, V Matti

2016 Volume 31, Issue 8, Page(s) 1375

MeSH term(s)	Glomerulosclerosis, Focal Segmental ; Humans ; Kidney Transplantation ; Plasmapheresis ; Recurrence
Language	English
Publishing date	2016
Publishing country	Germany
Document type	Letter ; Comment
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-015-3244-x
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Article ; Online: Genetics and CKD.

Vehaskari, V Matti

Advances in chronic kidney disease

2011 Volume 18, Issue 5, Page(s) 317–323

Abstract: The diagnosis of hereditary monogenic kidney diseases is frequently delayed, in part because of physicians' unfamiliarity with the relatively rare conditions or because of the late onset of symptoms in some patients. Molecular biology methods have ... ...

Abstract	The diagnosis of hereditary monogenic kidney diseases is frequently delayed, in part because of physicians' unfamiliarity with the relatively rare conditions or because of the late onset of symptoms in some patients. Molecular biology methods have clarified the underlying mutations in several types of CKD, and in the process have revealed previously unknown genes and pathogenetic pathways. Mutations affecting the integrity of the glomerular filtration barrier cause proteinuria or nephrotic syndrome; different types of Alport syndrome are caused by mutations in glomerular basement membrane type IV collagen; dysfunction of the primary cilium of tubule cells may lead to a variety of inherited progressive tubulointerstitial diseases; atypical hemolytic-uremic syndrome is frequently caused by inherited complement deficiencies; and progressive kidney injury develops in many inherited systemic or metabolic disorders. Some genetic diseases may not manifest until late childhood or adulthood. Accurate diagnosis is important for appropriate treatment, prognosis, genetic counseling, and possible renal transplantation.
MeSH term(s)	Chronic Disease ; Collagen Type IV/genetics ; Complement System Proteins/genetics ; Glomerular Filtration Barrier/pathology ; Glomerular Filtration Barrier/physiopathology ; Humans ; Kidney Tubules/pathology ; Kidney Tubules/physiopathology ; Mutation ; Nephritis, Hereditary/genetics ; Nephritis, Hereditary/pathology ; Nephritis, Interstitial/genetics ; Nephritis, Interstitial/pathology ; Nephrotic Syndrome/genetics ; Nephrotic Syndrome/pathology ; Proteinuria/genetics ; Uromodulin/genetics
Chemical Substances	Collagen Type IV ; Uromodulin ; Complement System Proteins (9007-36-7)
Language	English
Publishing date	2011-09
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1548-5609 ; 1548-5595
ISSN (online)	1548-5609
ISSN	1548-5595
DOI	10.1053/j.ackd.2011.07.001
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Article ; Online: Prenatal programming of kidney disease.

Vehaskari, V Matti

Current opinion in pediatrics

2010 Volume 22, Issue 2, Page(s) 176–182

Abstract: Purpose of review: To introduce the concept of prenatal programming; to discuss the emerging evidence that adverse prenatal environment programs increased risk of chronic kidney disease in the offspring in later life; to review the mechanism involved; ... ...

Abstract	Purpose of review: To introduce the concept of prenatal programming; to discuss the emerging evidence that adverse prenatal environment programs increased risk of chronic kidney disease in the offspring in later life; to review the mechanism involved; and to present potential intervention strategies. Recent findings: New observational studies in humans and studies in animal models have strengthened the association between low birth weight and chronic kidney disease in adulthood. The consequences of low birth weight are less obvious in children and young animals. A likely mechanism is that adverse intrauterine environment results in decreased final number of nephrons. The existing fewer glomeruli compensate by hyperfiltrating, which may accelerate the normal gradual age-related loss of nephrons throughout one's lifespan. Beginning life with a low nephron count may not cause morbidity during childhood because of the large functional reserve kidneys have, but as the count later falls below a critical level, chronic kidney disease may become manifest. Early life dietary factors may modify the risk. Summary: The charge for pediatricians is to identify children at risk, to counsel families to minimize any further renal risk factors such as smoking, obesity, and hypertension, and, in some cases together with a nephrologist, to institute pharmacologic therapy.
MeSH term(s)	Adult ; Birth Weight ; Female ; Humans ; Kidney Failure, Chronic/embryology ; Kidney Failure, Chronic/prevention & control ; Middle Aged ; Nephrons/pathology ; Pregnancy
Language	English
Publishing date	2010-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1049374-8
ISSN	1531-698X ; 1040-8703
ISSN (online)	1531-698X
ISSN	1040-8703
DOI	10.1097/MOP.0b013e328336ebc9
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Article: Programming of hypertension: the nervous kidney.

Vehaskari, V Matti

American journal of physiology. Renal physiology

2008 Volume 295, Issue 1, Page(s) F27–8

MeSH term(s)	Animals ; Female ; Humans ; Hypertension/etiology ; Kidney/innervation ; Kidney/physiopathology ; Pregnancy ; Prenatal Exposure Delayed Effects ; Stress, Physiological/complications
Language	English
Publishing date	2008-07
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	603837-2
ISSN	1522-1466 ; 1931-857X ; 0363-6127
ISSN (online)	1522-1466
ISSN	1931-857X ; 0363-6127
DOI	10.1152/ajprenal.90270.2008
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Article ; Online: Heritable forms of hypertension.

Vehaskari, V Matti

Pediatric nephrology (Berlin, Germany)

2009 Volume 24, Issue 10, Page(s) 1929–1937

Abstract: Among the causes of secondary hypertension are a group of disorders with a Mendelian inheritance pattern. Recent advances in molecular biology have unveiled the pathogenesis of hypertension in many of these conditions. Remarkably, the mechanism in every ... ...

Abstract	Among the causes of secondary hypertension are a group of disorders with a Mendelian inheritance pattern. Recent advances in molecular biology have unveiled the pathogenesis of hypertension in many of these conditions. Remarkably, the mechanism in every case has proved to be upregulation of sodium (Na) reabsorption in the distal nephron, with accompanying expansion of extracellular volume. In one group, the mutations involve the Na-transport machinery in distal tubule cells themselves: the distal convoluted tubule (DCT) cell and the principal cell of the collecting duct. Examples include Liddle's syndrome, with an activating mutation of epithelial Na channel (ENaC); two types of Gordon's syndrome, with mutations in two regulatory kinases [with no lysine (K) serine/threonine protein kinases (WNK)1 or WNK4]; and apparent mineralocorticoid excess (AME), with an inactivating mutation in the glucocorticoid-metabolizing 11beta-hydroxysteroid dehydrogenase type 2 enzyme (11HD2). In another group, abnormal adrenal steroid production leads to inappropriate stimulation of the mineralocorticoid receptor (MR) in the distal nephron. The pathophysiology may involve inappropriate production of aldosterone [in glucocorticoid-remediable aldosteronism (GRA) and familial hyperaldosteronism type II (FH II)], of cortisol (in familial glucocorticoid resistance), or of other steroid metabolites (in congenital adrenal hyperplasia and GRA). In contrast to earlier beliefs, hypertension in many of the inherited disorders may be mild, and electrolyte and acid-base abnormalities are often not present. Monogenic hypertension should therefore enter the differential diagnosis of any child or adolescent with hypertension. Plasma renin activity (PRA) is the appropriate screening tool for all types of inherited hypertension.
MeSH term(s)	Adrenal Cortex Diseases/complications ; Adrenal Cortex Diseases/metabolism ; Adrenal Cortex Diseases/physiopathology ; Child ; Humans ; Hypertension/congenital ; Hypertension/genetics ; Hypertension/physiopathology ; Kidney Diseases/complications ; Kidney Diseases/metabolism ; Kidney Diseases/physiopathology ; Sodium/metabolism
Chemical Substances	Sodium (9NEZ333N27)
Language	English
Publishing date	2009-10
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-007-0537-8
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Article: Developmental origins of adult hypertension: new insights into the role of the kidney.

Vehaskari, V Matti

Pediatric nephrology (Berlin, Germany)

2007 Volume 22, Issue 4, Page(s) 490–495

Abstract: It is now accepted that early life environment can modulate adult phenotype. One of the best documented examples is the effect of prenatal environment on adult hypertension and cardiovascular morbidity. Human epidemiologic studies have been complemented ... ...

Abstract	It is now accepted that early life environment can modulate adult phenotype. One of the best documented examples is the effect of prenatal environment on adult hypertension and cardiovascular morbidity. Human epidemiologic studies have been complemented with experimental models showing, for example, that maternal dietary manipulations during pregnancy in the rat can be used to induce adult hypertension in the offspring. The weight of the emerging evidence suggests that abnormal Na handling by the kidney plays an important role in the pathogenesis of the hypertension. Although the number of nephrons is modestly reduced in most experimental models, there is very little change in total glomerular filtration rate, casting doubt on the hypothesis that restricted Na filtration is the major mechanism. Recent studies have instead strongly suggested that renal tubular handling of Na is altered, resulting in an altered set-point for Na balance. The mechanism may involve intrarenal inflammation and increased oxidative stress which disrupt the tubulointerstitial microenvironment, leading to constitutively upregulated Na reabsorption in the distal tubule. The upregulation may be mediated by autocrine and paracrine factors promoting distal tubule Na reabsorption. A similar mechanism has been hypothesized to be important in other types of hypertension and may hence be a common pathway in the genesis of volume-dependent hypertension.
MeSH term(s)	Adult ; Glomerular Filtration Rate ; Humans ; Hypertension/physiopathology ; Kidney/embryology ; Kidney/physiopathology ; Nephrons
Language	English
Publishing date	2007-04
Publishing country	Germany
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-006-0353-6
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Article ; Online: Uromodulin: old friend with new roles in health and disease.

Iorember, Franca M / Vehaskari, V Matti

Pediatric nephrology (Berlin, Germany)

2013 Volume 29, Issue 7, Page(s) 1151–1158

Abstract: The most abundant urinary protein, Tamm-Horsfall protein, later renamed uromodulin, is expressed exclusively by the thick ascending limb cells of the kidney and released into urine from the apical cell membrane. Uromodulin is believed to protect against ... ...

Abstract	The most abundant urinary protein, Tamm-Horsfall protein, later renamed uromodulin, is expressed exclusively by the thick ascending limb cells of the kidney and released into urine from the apical cell membrane. Uromodulin is believed to protect against urinary tract infections and stones, but its other physiologic functions have remained obscure until recently. Renewed interest in uromodulin has been brought about by the identification of uromodulin mutations as causes of a discrete group of diseases that are distinct from nephronophthisis. The three overlapping clinical uromodulin-associated kidney diseases (UAKD) are medullary cystic disease type 2, familial juvenile hyperuricemic nephropathy and glomerulocystic kidney disease. Previously thought of as "adult diseases", it is now recognized that they may also present in childhood and even in infancy. Common characteristics of all three diseases are autosomal dominant inheritance, unremarkable urine sediment and slow progression to end-stage renal disease (ESRD). They are frequently associated with hyperuricemia and gout. These diseases appear to result from failure of the mutant uromodulin to be incorporated into the apical cilium, thereby placing UAKD in the category of "ciliopathies". In addition to causing specific UAKD, certain uromodulin gene polymorphisms have been linked to ESRD in general, suggesting that uromodulin plays a modulatory role in kidney disease progression.
MeSH term(s)	Animals ; Central Nervous System Diseases/etiology ; Dental Enamel/abnormalities ; Diabetes Mellitus, Type 2/etiology ; Gout/etiology ; Humans ; Hyperuricemia/etiology ; Kidney Diseases/etiology ; Kidney Diseases, Cystic/etiology ; Mutation ; Polycystic Kidney, Autosomal Dominant/etiology ; Renal Insufficiency, Chronic/etiology ; Uromodulin/chemistry ; Uromodulin/deficiency ; Uromodulin/genetics ; Uromodulin/physiology
Chemical Substances	Uromodulin
Language	English
Publishing date	2013-07-24
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-013-2563-z
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Article ; Online: Increased Autophagy and Apoptosis in the Kidneys of Intrauterine Growth Restricted Rats.

Stewart, Tyrus / Kallash, Mahmoud / Vehaskari, V Matti / Hodgeson, Sydney M / Aviles, Diego H

Fetal and pediatric pathology

2019 Volume 38, Issue 3, Page(s) 185–194

Abstract: Background: IUGR has been associated with nephron loss and chronic kidney disease (CKD).: Materials and methods: We examined autophagy and apoptosis markers in the kidneys of IUGR Sprague Dawley rats induced by maternal low protein diet (LP), ... ...

Abstract	Background: IUGR has been associated with nephron loss and chronic kidney disease (CKD). Materials and methods: We examined autophagy and apoptosis markers in the kidneys of IUGR Sprague Dawley rats induced by maternal low protein diet (LP), comparing them to controls. The autophagy marker LC3B, the pro-apoptotic protein Bax, and the anti-apoptotic protein Bcl-2 were determined by quantitative immunoblotting. Immunohistochemical expressions of LC3B, Bax, and Bcl-2 were evaluated at 4 weeks age. Glomerular counts (by maceration techniques) were performed at 5 weeks. Results: The LP diet offspring were lighter (P < 0.05). In IUGR kidneys, LC3B and Bax were increased at birth (p < 0.05, p < 0.001) and at 4 weeks (p < 0.0142, p < 0.0001), Bcl-2 was decreased at birth (p < 0.05), and there were less glomeruli (p < 0.01) at 5 weeks. Conclusions: Autophagy and apoptosis may have a role in IUGR associated decreased nephron number in Sprague rats.
MeSH term(s)	Animals ; Apoptosis/physiology ; Autophagy/physiology ; Diet, Protein-Restricted ; Female ; Fetal Growth Retardation/pathology ; Kidney/metabolism ; Kidney/pathology ; Kidney Glomerulus/metabolism ; Rats, Sprague-Dawley
Language	English
Publishing date	2019-02-11
Publishing country	England
Document type	Journal Article
ZDB-ID	2165508-X
ISSN	1551-3823 ; 1551-3815 ; 1522-7952
ISSN (online)	1551-3823
ISSN	1551-3815 ; 1522-7952
DOI	10.1080/15513815.2018.1564160
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Article: Inherited Na transport disorders: the taming of the syndromes.

Vehaskari, V Matti

Current opinion in pediatrics

2004 Volume 16, Issue 2, Page(s) 182–187

Abstract: Purpose of review: The study of inherited renal sodium (Na) transport disorders has greatly benefited from the use of new molecular biology research tools. This review discusses the recent findings that have expanded our knowledge and may impact ... ...

Abstract	Purpose of review: The study of inherited renal sodium (Na) transport disorders has greatly benefited from the use of new molecular biology research tools. This review discusses the recent findings that have expanded our knowledge and may impact clinical decision-making. Recent findings: The genetic and molecular biology diagnostic tools have to a large extent validated conclusions drawn from physiologic studies that documented suppressed or enhanced Na transport in specific distal nephron segments in various disorders. However, many surprises were also encountered. In several conditions, no mutation in the Na transporter itself was found despite apparent dysfunction of the transporter. Further search has led to discovery of additional mechanisms. Some involve mutations in other transporters, especially potassium (K) and chloride (Cl) channels, which secondarily affect function of the Na transporter by altering electrochemical gradients across the cell membrane. Examples include certain types of Bartter syndrome. In other patients, search for mechanism has led to discovery of novel physiologic regulatory pathways that, if abnormal, will lead to up- or downregulation of an Na transporter. Examples include some types of Bartter syndrome and Gordon syndrome. Genetic diagnosis has also revealed hitherto unexplained phenotypic heterogeneity between patients carrying the same mutation, implying a contributory role for other factors. Summary: Genetic and molecular diagnosis will have an expanding role in the understanding and management of the Na transport disorders. Predicting prognosis and inheritance pattern, as well as treatment plans will in the future be based on genetic diagnosis.
MeSH term(s)	Biological Transport, Active ; Cell Membrane/metabolism ; Humans ; Metal Metabolism, Inborn Errors/genetics ; Metal Metabolism, Inborn Errors/metabolism ; Sodium/metabolism ; Syndrome
Chemical Substances	Sodium (9NEZ333N27)
Language	English
Publishing date	2004-06-28
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1049374-8
ISSN	1531-698X ; 1040-8703
ISSN (online)	1531-698X
ISSN	1040-8703
DOI	10.1097/00008480-200404000-00012
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Article ; Online: Recurrence of granulomatous interstitial nephritis in transplanted kidney.

Vargas, Federico / Gedalia, Abraham / Craver, Randall D / Matti Vehaskari, V

Pediatric transplantation

2010 Volume 14, Issue 5, Page(s) e54–7

Abstract: Sarcoidosis is a multisystemic disease of unknown etiology. Minor renal involvement is not rare but kidney failure is uncommon and only rare cases of recurrent disease in a kidney transplant have been published. We report a patient who at age 10 yr ... ...

Abstract	Sarcoidosis is a multisystemic disease of unknown etiology. Minor renal involvement is not rare but kidney failure is uncommon and only rare cases of recurrent disease in a kidney transplant have been published. We report a patient who at age 10 yr developed ESRD secondary to renal sarcoidosis with GIN. Her disease subsequently recurred in the transplanted kidney despite standard immunosuppression with prednisone, tacrolimus, and mycophenolate mofetil. The recurrent disease appeared to respond to increased immunosuppression, which included infliximab. However, the patient died of disseminated histoplasmosis three yr post-transplant.
MeSH term(s)	Adolescent ; Fatal Outcome ; Female ; Humans ; Immunosuppressive Agents/therapeutic use ; Kidney Failure, Chronic ; Kidney Transplantation ; Nephritis, Interstitial/drug therapy ; Nephritis, Interstitial/etiology ; Nephritis, Interstitial/pathology ; Nephritis, Interstitial/surgery ; Recurrence ; Sarcoidosis/complications
Chemical Substances	Immunosuppressive Agents
Language	English
Publishing date	2010-08
Publishing country	Denmark
Document type	Case Reports ; Journal Article
ZDB-ID	1390284-2
ISSN	1399-3046 ; 1397-3142
ISSN (online)	1399-3046
ISSN	1397-3142
DOI	10.1111/j.1399-3046.2009.01173.x
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