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Article: Synergism between hydrogen sulfide (H(2)S) and nitric oxide (NO) in vasorelaxation induced by stonustoxin (SNTX), a lethal and hypotensive protein factor isolated from stonefish Synanceja horrida venom.

Liew, H C / Khoo, H E / Moore, P K / Bhatia, M / Lu, J / Moochhala, S M

2007 Volume 80, Issue 18, Page(s) 1664–1668

Abstract: ... inhibited SNTX-induced vasorelaxation, indicating that H(2)S may also play a part in the effect of SNTX ... The combined use of L-NAME with PAG or BCA showed that H(2)S and NO act synergistically in effecting SNTX ...

Abstract	Stonustoxin (SNTX) is a 148 kDa, dimeric, hypotensive and lethal protein factor isolated from the venom of the stonefish Synanceja horrida. SNTX (10-320 ng/ml) progressively causes relaxation of endothelium-intact, phenylephrine (PE)-precontracted rat thoracic aortic rings. The SNTX-induced vasorelaxation was inhibited by L-N(G)-nitro arginine methyl ester (L-NAME), suggesting that nitric oxide (NO) contributes to the SNTX-induced response. Interestingly, D, L-proparglyglycine (PAG) and beta-cyano-L-alanine (BCA), irreversible and competitive inhibitors of cystathionine-gamma-lyase (CSE) respectively, also inhibited SNTX-induced vasorelaxation, indicating that H(2)S may also play a part in the effect of SNTX. The combined use of L-NAME with PAG or BCA showed that H(2)S and NO act synergistically in effecting SNTX-induced vasorelaxation.
MeSH term(s)	Animals ; Aorta, Thoracic/metabolism ; Cystathionine gamma-Lyase/antagonists & inhibitors ; Enzyme Inhibitors/pharmacology ; Fish Venoms/isolation & purification ; Fish Venoms/pharmacology ; Fishes, Poisonous ; Hydrogen Sulfide/agonists ; Hydrogen Sulfide/metabolism ; Male ; Nitric Oxide/agonists ; Nitric Oxide/metabolism ; Organ Culture Techniques ; Phenylephrine/pharmacology ; Rats ; Rats, Sprague-Dawley ; Vasoconstrictor Agents/pharmacology ; Vasodilation/drug effects
Chemical Substances	Enzyme Inhibitors ; Fish Venoms ; Vasoconstrictor Agents ; stonustoxin (137803-80-6) ; Phenylephrine (1WS297W6MV) ; Nitric Oxide (31C4KY9ESH) ; Cystathionine gamma-Lyase (EC 4.4.1.1) ; Hydrogen Sulfide (YY9FVM7NSN)
Language	English
Publishing date	2007-04-10
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2007.01.058
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Article ; Online: Early renal failure in childhood in a male with Fabry disease.

Hogh, Josephine Norre / Ebrahim, Hatim / Moochhala, Shabbir / Ramaswami, Uma

BMJ case reports

2022 Volume 15, Issue 5

Abstract: Fabry disease is an X-linked lysosomal storage disorder caused by reduced activity or absence of the alpha-galactosidase A enzyme resulting in systemic accumulation of glycosphingolipids. End-stage renal disease (ESRD) is a late-stage manifestation of ... ...

Abstract	Fabry disease is an X-linked lysosomal storage disorder caused by reduced activity or absence of the alpha-galactosidase A enzyme resulting in systemic accumulation of glycosphingolipids. End-stage renal disease (ESRD) is a late-stage manifestation of Fabry disease, typically presenting in the fifth decade of life, but is very rare in childhood. Here we present a case of an 11-year-old boy with classical Fabry disease presenting with ESRD requiring haemodialysis and transplant. Diagnosis was confirmed by renal biopsy,
MeSH term(s)	Alleles ; Child ; Fabry Disease/complications ; Fabry Disease/diagnosis ; Fabry Disease/genetics ; Female ; Humans ; Kidney Failure, Chronic/complications ; Kidney Failure, Chronic/therapy ; Male ; Mutation ; alpha-Galactosidase/genetics
Chemical Substances	alpha-Galactosidase (EC 3.2.1.22)
Language	English
Publishing date	2022-05-10
Publishing country	England
Document type	Case Reports ; Journal Article
ISSN	1757-790X
ISSN (online)	1757-790X
DOI	10.1136/bcr-2021-246682
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Article ; Online: Rare variants in the sodium-dependent phosphate transporter gene SLC34A3 explain missing heritability of urinary stone disease.

Sadeghi-Alavijeh, Omid / Chan, Melanie M Y / Moochhala, Shabbir H / Howles, Sarah / Gale, Daniel P / Böckenhauer, Detlef

Kidney international

2023 Volume 104, Issue 5, Page(s) 975–984

Abstract: Urinary stone disease (USD) is a major health burden affecting over 10% of the United Kingdom population. While stone disease is associated with lifestyle, genetic factors also strongly contribute. Common genetic variants at multiple loci from genome- ... ...

Abstract	Urinary stone disease (USD) is a major health burden affecting over 10% of the United Kingdom population. While stone disease is associated with lifestyle, genetic factors also strongly contribute. Common genetic variants at multiple loci from genome-wide association studies account for 5% of the estimated 45% heritability of the disorder. Here, we investigated the extent to which rare genetic variation contributes to the unexplained heritability of USD. Among participants of the United Kingdom 100,000-genome project, 374 unrelated individuals were identified and assigned diagnostic codes indicative of USD. Whole genome gene-based rare variant testing and polygenic risk scoring against a control population of 24,930 ancestry-matched controls was performed. We observed (and replicated in an independent dataset) exome-wide significant enrichment of monoallelic rare, predicted damaging variants in the SLC34A3 gene for a sodium-dependent phosphate transporter that were present in 5% cases compared with 1.6% of controls. This gene was previously associated with autosomal recessive disease. The effect on USD risk of having a qualifying SLC34A3 variant was greater than that of a standard deviation increase in polygenic risk derived from GWAS. Addition of the rare qualifying variants in SLC34A3 to a linear model including polygenic score increased the liability-adjusted heritability from 5.1% to 14.2% in the discovery cohort. We conclude that rare variants in SLC34A3 represent an important genetic risk factor for USD, with effect size intermediate between the fully penetrant rare variants linked with Mendelian disorders and common variants associated with USD. Thus, our findings explain some of the heritability unexplained by prior common variant genome-wide association studies.
MeSH term(s)	Humans ; Genetic Predisposition to Disease ; Genome-Wide Association Study ; Polymorphism, Single Nucleotide ; Sodium ; Sodium-Phosphate Cotransporter Proteins, Type IIc/genetics ; Urinary Calculi/genetics ; Urolithiasis/genetics ; Urologic Diseases
Chemical Substances	SLC34A3 protein, human ; Sodium (9NEZ333N27) ; Sodium-Phosphate Cotransporter Proteins, Type IIc
Language	English
Publishing date	2023-07-04
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2023.06.019
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Zs.A 797: Show issues

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Article: Extracellular Pyrophosphate in the Kidney: How Does It Get There and What Does It Do

Moochhala, Shabbir H.

Nephron Physiology

2012 Volume 120, Issue 4, Page(s) p33–p38

Abstract: ... yet other ANK mutations do not cause a renal phenotype. Despite evidence over 10 years of ANKH’s involvement ...

Institution	UCL Centre for Nephrology Royal Free, Royal Free London NHS Foundation Trust, London, UK
Abstract	Pyrophosphate (PPi) is well known as a regulator of calcification, and the ANKH (ANK in mouse) protein has a role in the membrane transport of PPi. Earlier work concentrated on bones and joints, but ANKH is also likely to have important roles in the kidney, with newer studies focusing on vascular calcification in renal failure. Renal calcification can occur due to a naturally occurring ANK mouse mutation, yet other ANK mutations do not cause a renal phenotype. Despite evidence over 10 years of ANKH’s involvement in PPi transport, efflux of PPi via ANKH has never been demonstrated. Rather than physically moving PPi, the ANKH protein may assist its membrane transport in other ways such as by hydrolysis and compartmentalisation. Protein complexes may account for effects of ANKH that are specific to particular tissues. In the kidney, recent localisation data may be helpful in suggesting physiological roles for ANKH, such as its co-localisation with aquaporin-2 and cilial proteins. Such diverse functions would reflect the ubiquitous nature of ANKH in tissues and its profound evolutionary conservation.
Keywords	Pyrophosphate ; ANKH ; ANK ; Membrane transport ; Efflux ; Calcification
Language	English
Publishing date	2012-10-12
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Minireview
ZDB-ID	207121-6
ISSN	1660-2137 ; 1423-0186 ; 2235-3186 ; 1660-8151 ; 0028-2766
ISSN (online)	1660-2137 ; 1423-0186 ; 2235-3186
ISSN	1660-8151 ; 0028-2766
DOI	10.1159/000341597
Database	Karger publisher's database

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Article ; Online: Extracellular Pyrophosphate in the Kidney: How Does It Get There and What Does It Do?

Moochhala, Shabbir H.

Nephron Physiology

2012 Volume 120, Issue 4, Page(s) p33–p38

Abstract: ... yet other ANK mutations do not cause a renal phenotype. Despite evidence over 10 years of ANKH’s involvement ...

Abstract	Pyrophosphate (PPi) is well known as a regulator of calcification, and the ANKH (ANK in mouse) protein has a role in the membrane transport of PPi. Earlier work concentrated on bones and joints, but ANKH is also likely to have important roles in the kidney, with newer studies focusing on vascular calcification in renal failure. Renal calcification can occur due to a naturally occurring ANK mouse mutation, yet other ANK mutations do not cause a renal phenotype. Despite evidence over 10 years of ANKH’s involvement in PPi transport, efflux of PPi via ANKH has never been demonstrated. Rather than physically moving PPi, the ANKH protein may assist its membrane transport in other ways such as by hydrolysis and compartmentalisation. Protein complexes may account for effects of ANKH that are specific to particular tissues. In the kidney, recent localisation data may be helpful in suggesting physiological roles for ANKH, such as its co-localisation with aquaporin-2 and cilial proteins. Such diverse functions would reflect the ubiquitous nature of ANKH in tissues and its profound evolutionary conservation.
Keywords	Pyrophosphate ; ANKH ; ANK ; Membrane transport ; Efflux ; Calcification
Language	English
Publisher	S. Karger AG
Publishing place	Basel
Publishing country	Switzerland
Document type	Article ; Online
ZDB-ID	207121-6
ISSN	1660-2137 ; 1423-0186 ; 0028-2766 ; 1660-8151 ; 1660-2137 ; 0028-2766 ; 1660-8151
ISSN (online)	1660-2137 ; 1423-0186
ISSN	1660-2137 ; 0028-2766 ; 1660-8151
DOI	10.1159/000341597
Database	Karger publisher's database

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Article ; Online: ePHex: a phase 3, double-blind, placebo-controlled, randomized study to evaluate long-term efficacy and safety of Oxalobacter formigenes in patients with primary hyperoxaluria.

Ariceta, Gema / Collard, Laure / Abroug, Saoussen / Moochhala, Shabbir H / Gould, Edward / Boussetta, Abir / Ben Hmida, Mohamed / De, Sudarsana / Hunley, Tracy E / Jarraya, Faical / Fraga, Gloria / Banos, Ana / Lindner, Elisabeth / Dehmel, Bastian / Schalk, Gesa

Pediatric nephrology (Berlin, Germany)

2022

Abstract: Background: Primary hyperoxalurias (PHs) are rare genetic diseases that increase the endogenous level of oxalate, a waste metabolite excreted predominantly by the kidneys and also the gut. Treatments aim to improve oxalate excretion, or reduce oxalate ... ...

Abstract	Background: Primary hyperoxalurias (PHs) are rare genetic diseases that increase the endogenous level of oxalate, a waste metabolite excreted predominantly by the kidneys and also the gut. Treatments aim to improve oxalate excretion, or reduce oxalate generation, to prevent kidney function deterioration. Oxalobacter formigenes is an oxalate metabolizing bacterium. This Phase III, double-blind, placebo-controlled randomized trial investigated the effectiveness of orally administered Oxabact™, a lyophilized O. formigenes formulation, at reducing plasma oxalate levels in patients suffering from PH. Methods: Subjects (≥ 2 years of age) with a diagnosis of PH and maintained but suboptimal kidney function (mean estimated glomerular filtration rate at baseline < 90 mL/min/1.73 m Results: Forty-three subjects were screened, 25 were recruited and one was discontinued. At Week 52, O. formigenes was established in the gut of subjects receiving Oxabact. Despite decreasing plasma oxalate level in subjects treated with Oxabact, and stable/increased levels with placebo, there was no significant difference between groups in the primary outcome (Least Squares mean estimate of treatment difference was - 3.80 μmol/L; 95% CI: - 7.83, 0.23; p-value = 0.064). Kidney function remained stable in both treatments. Conclusions: Oxabact treatment may have stabilized/reduced plasma oxalate versus a rise with placebo, but the difference over 12 months was not statistically significant (p = 0.06). A subtle effect observed with Oxabact suggests that O. formigenes may aid in preventing kidney stones. A higher resolution version of the Graphical abstract is available as Supplementary information.
Language	English
Publishing date	2022-05-12
Publishing country	Germany
Document type	Journal Article
ZDB-ID	631932-4
ISSN	1432-198X ; 0931-041X
ISSN (online)	1432-198X
ISSN	0931-041X
DOI	10.1007/s00467-022-05591-5
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Article ; Online: Determinants of Kidney Failure in Primary Hyperoxaluria Type 1: Findings of the European Hyperoxaluria Consortium.

Metry, Elisabeth L / Garrelfs, Sander F / Deesker, Lisa J / Acquaviva, Cecile / D'Ambrosio, Viola / Bacchetta, Justine / Beck, Bodo B / Cochat, Pierre / Collard, Laure / Hogan, Julien / Ferraro, Pietro Manuel / Franssen, Casper F M / Harambat, Jérôme / Hulton, Sally-Anne / Lipkin, Graham W / Mandrile, Giorgia / Martin-Higueras, Cristina / Mohebbi, Nilufar / Moochhala, Shabbir H /

Neuhaus, Thomas J / Prikhodina, Larisa / Salido, Eduardo / Topaloglu, Rezan / Oosterveld, Michiel J S / Groothoff, Jaap W / Peters-Sengers, Hessel

Kidney international reports

2023 Volume 8, Issue 10, Page(s) 2029–2042

Abstract: Introduction: Primary hyperoxaluria type 1 (PH1) has a highly heterogeneous disease course. Apart from the c.508G>A (p.Gly170Arg) : Methods: In this retrospective study of 932 patients with PH1 included in the OxalEurope registry, we analyzed ... ...

Abstract	Introduction: Primary hyperoxaluria type 1 (PH1) has a highly heterogeneous disease course. Apart from the c.508G>A (p.Gly170Arg) Methods: In this retrospective study of 932 patients with PH1 included in the OxalEurope registry, we analyzed genotype-phenotype correlations as well as the impact of nephrocalcinosis, urolithiasis, and urinary oxalate and glycolate excretion on the development of kidney failure, using survival and mixed model analyses. Results: The risk of developing kidney failure was the highest for 175 vitamin-B6 unresponsive ("null") homozygotes and lowest for 155 patients with c.508G>A and c.454T>A (p.Phe152Ile) variants, with a median age of onset of kidney failure of 7.8 and 31.8 years, respectively. Fifty patients with c.731T>C (p.Ile244Thr) homozygote variants had better kidney survival than null homozygotes ( Conclusion: In conclusion, homozygosity for
Language	English
Publishing date	2023-08-04
Publishing country	United States
Document type	Journal Article
ISSN	2468-0249
ISSN (online)	2468-0249
DOI	10.1016/j.ekir.2023.07.025
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Article ; Online: PHYOX2: a pivotal randomized study of nedosiran in primary hyperoxaluria type 1 or 2.

Kidney international

2022 Volume 103, Issue 1, Page(s) 207–217

Abstract: Nedosiran is an investigational RNA interference agent designed to inhibit expression of hepatic lactate dehydrogenase, the enzyme thought responsible for the terminal step of oxalate synthesis. Oxalate overproduction is the hallmark of all genetic ... ...

Abstract	Nedosiran is an investigational RNA interference agent designed to inhibit expression of hepatic lactate dehydrogenase, the enzyme thought responsible for the terminal step of oxalate synthesis. Oxalate overproduction is the hallmark of all genetic subtypes of primary hyperoxaluria (PH). In this double-blind, placebo-controlled study, we randomly assigned (2:1) 35 participants with PH1 (n = 29) or PH2 (n = 6) with eGFR ≥30 mL/min/1.73 m
MeSH term(s)	Humans ; Hyperoxaluria/urine ; Hyperoxaluria, Primary/diagnosis ; Hyperoxaluria, Primary/drug therapy ; Hyperoxaluria, Primary/genetics ; Oxalates/metabolism ; RNA Interference ; Double-Blind Method
Chemical Substances	nedosiran ; Oxalates
Language	English
Publishing date	2022-08-22
Publishing country	United States
Document type	Randomized Controlled Trial ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1016/j.kint.2022.07.025
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Zs.A 797: Show issues

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Article ; Online: Long-Term Transplantation Outcomes in Patients With Primary Hyperoxaluria Type 1 Included in the European Hyperoxaluria Consortium (OxalEurope) Registry.

Kidney international reports

2021 Volume 7, Issue 2, Page(s) 210–220

Abstract: Introduction: In primary hyperoxaluria type 1 (PH1), oxalate overproduction frequently causes kidney stones, nephrocalcinosis, and kidney failure. As PH1 is caused by a congenital liver enzyme defect, combined liver-kidney transplantation (CLKT) has ... ...

Abstract	Introduction: In primary hyperoxaluria type 1 (PH1), oxalate overproduction frequently causes kidney stones, nephrocalcinosis, and kidney failure. As PH1 is caused by a congenital liver enzyme defect, combined liver-kidney transplantation (CLKT) has been recommended in patients with kidney failure. Nevertheless, systematic analyses on long-term transplantation outcomes are scarce. The merits of a sequential over combined procedure regarding kidney graft survival remain unclear as is the place of isolated kidney transplantation (KT) for patients with vitamin B6-responsive genotypes. Methods: We used the OxalEurope registry for retrospective analyses of patients with PH1 who underwent transplantation. Analyses of crude Kaplan-Meier survival curves and adjusted relative hazards from the Cox proportional hazards model were performed. Results: A total of 267 patients with PH1 underwent transplantation between 1978 and 2019. Data of 244 patients (159 CLKTs, 48 isolated KTs, 37 sequential liver-KTs [SLKTs]) were eligible for comparative analyses. Comparing CLKTs with isolated KTs, adjusted mortality was similar in patients with B6-unresponsive genotypes but lower after isolated KT in patients with B6-responsive genotypes (adjusted hazard ratio 0.07, 95% CI: 0.01-0.75, Conclusion: The CLKT or SLKT remains the preferred transplantation modality in patients with PH1 with B6-unresponsive genotypes, but isolated KT could be an alternative approach in patients with B6-responsive genotypes.
Language	English
Publishing date	2021-11-26
Publishing country	United States
Document type	Journal Article
ISSN	2468-0249
ISSN (online)	2468-0249
DOI	10.1016/j.ekir.2021.11.006
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Article: How we estimate GFR--a pitfall of using a serum creatinine-based formula.

Refaie, R / Moochhala, S H / Kanagasundaram, N S

Clinical nephrology

2007 Volume 68, Issue 4, Page(s) 235–237

Abstract: Chronic kidney disease (CKD) is defined using the estimated glomerular filtration rate (eGFR). This has led to a large increase in the diagnosis of CKD in the United Kingdom, the majority of which is in its earlier stages and is detected in non-hospital ... ...

Abstract	Chronic kidney disease (CKD) is defined using the estimated glomerular filtration rate (eGFR). This has led to a large increase in the diagnosis of CKD in the United Kingdom, the majority of which is in its earlier stages and is detected in non-hospital settings. It is important to be aware that eGFR calculations will reflect inaccuracies in the measured serum creatinine, as the latter is an important component of the calculation. We report a case in which a patient with high muscle-mass who had consumed large quantities of a creatine-containing nutritional supplement presented with apparently reduced renal function on the basis of the serum creatinine and therefore also the eGFR calculation (MDRD equation). Creatine is an amino acid which is a precursor of creatinine, and is known to transiently increase serum creatinine. 6 weeks after discontinuing creatine ingestion, serum creatinine had fallen but still gave rise to an apparently abnormal calculated eGFR. In fact, renal function was shown to be normal when estimated using 24-hour urinary creatinine clearance. This case demonstrates that the upper extreme of muscle mass and ingestion of creatine can affect not only serum creatinine but also the calculated eGFR. Knowledge of common confounding factors and their effects on serum creatinine and eGFR will allow appreciation of the limitations of these measures of renal function, and can prevent unnecessary over-investigation of such patients.
MeSH term(s)	Adult ; Creatine/administration & dosage ; Creatine/poisoning ; Creatinine/blood ; Diagnosis, Differential ; Dietary Supplements/poisoning ; Glomerular Filtration Rate/drug effects ; Humans ; Male ; Poisoning/diagnosis ; Renal Insufficiency, Chronic/chemically induced ; Renal Insufficiency, Chronic/diagnosis
Chemical Substances	Creatinine (AYI8EX34EU) ; Creatine (MU72812GK0)
Language	English
Publishing date	2007-10-30
Publishing country	Germany
Document type	Case Reports ; Journal Article
ZDB-ID	185101-9
ISSN	0301-0430
ISSN	0301-0430
DOI	10.5414/cnp68235
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