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  1. Article ; Online: Capitellum Osteochondral Allograft Transplantation for Osteochondritis Dissecans of the Elbow.

    Samuelsen, Brian / Grantham, W Jeffrey / Goldenberg, Brandon / Dey Hazra, Rony-Orijit / Dey Hazra, Maria E / Hanson, Jared A / Millett, Peter J

    The Journal of hand surgery

    2023  Volume 48, Issue 11, Page(s) 1165.e1–1165.e6

    Abstract: Reconstruction of unstable osteochondritis dissecans lesions of the capitellum using fresh osteochondral allograft transplantation from the capitellum has the advantages of restoring hyaline cartilage, matching the native radius of curvature, and ... ...

    Abstract Reconstruction of unstable osteochondritis dissecans lesions of the capitellum using fresh osteochondral allograft transplantation from the capitellum has the advantages of restoring hyaline cartilage, matching the native radius of curvature, and avoiding the donor-site morbidity encountered with osteochondral autograft transfer. This technical note describes the indications and contraindications, pertinent anatomy, and surgical technique of open osteochondral allograft transplantation using fresh distal humerus allograft for the treatment of unstable osteochondritis dissecans lesions of the capitellum.
    MeSH term(s) Humans ; Osteochondritis Dissecans/surgery ; Elbow ; Treatment Outcome ; Elbow Joint/surgery ; Elbow Joint/pathology ; Transplantation, Autologous ; Bone Transplantation/methods ; Allografts
    Language English
    Publishing date 2023-03-24
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 605716-0
    ISSN 1531-6564 ; 0363-5023
    ISSN (online) 1531-6564
    ISSN 0363-5023
    DOI 10.1016/j.jhsa.2023.01.020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1431: Show issues Location:
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  2. Article ; Online: Rationale for early treatment of polycystic kidney disease.

    Grantham, Jared J

    Pediatric nephrology (Berlin, Germany)

    2014  Volume 30, Issue 7, Page(s) 1053–1062

    Abstract: In hereditary cystic disorders, renal injury begins with the formation of the first cyst. Renal injury may manifest as large kidneys, abdominal pain, hypertension and hematuria in children and young adults with autosomal dominant polycystic kidney ... ...

    Abstract In hereditary cystic disorders, renal injury begins with the formation of the first cyst. Renal injury may manifest as large kidneys, abdominal pain, hypertension and hematuria in children and young adults with autosomal dominant polycystic kidney disease (ADPKD). In autosomal recessive PKD (ARPKD) and ADPKD, cysts form primarily in collecting ducts and expand progressively. Collecting duct cysts that block urine flow have the potential to block urine formation in large numbers of upstream nephrons. In an ARPKD rat congenitally lacking vasopressin, only a few cysts developed until exogenous arginine vasopressin (AVP) was administered. AVP elevates cyclic AMP in vulnerable tubule cells to stimulate mitogenesis and fluid secretion, thereby causing cysts to form and enlarge indefinitely. The administration of an AVP-V2 receptor inhibitor or the consumption of sufficient water to persistently lower plasma AVP levels will ameliorate disease progression. Renal volume measurements provide the most reliable way to forecast long-term outcome in individual children and adult patients with ADPKD. Many drugs that have demonstrated efficacy in small clinical trials, preclinical trials and cell-based studies are in the treatment pipeline. Counseling, regular exercise, limitation of dietary calories, salt, protein and fat, increased fluid intake throughout the day and treatment of hypertension are components of a rational treatment program that can be offered at an early age to those with, or at risk for developing PKD.
    MeSH term(s) Adult ; Animals ; Child ; Disease Progression ; Early Diagnosis ; Humans ; Polycystic Kidney Diseases/genetics ; Polycystic Kidney Diseases/pathology ; Polycystic Kidney Diseases/therapy ; Polycystic Kidney, Autosomal Dominant/genetics ; Polycystic Kidney, Autosomal Dominant/pathology ; Polycystic Kidney, Autosomal Dominant/therapy ; Polycystic Kidney, Autosomal Recessive/genetics ; Polycystic Kidney, Autosomal Recessive/pathology ; Polycystic Kidney, Autosomal Recessive/therapy ; Rats ; TRPP Cation Channels/genetics
    Chemical Substances TRPP Cation Channels ; polycystic kidney disease 1 protein
    Language English
    Publishing date 2014-07-15
    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/s00467-014-2882-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Solitary renal cysts: worth a second look?

    Grantham, Jared J

    American journal of kidney diseases : the official journal of the National Kidney Foundation

    2012  Volume 59, Issue 5, Page(s) 593–594

    MeSH term(s) Female ; Humans ; Kidney Diseases, Cystic/diagnostic imaging ; Kidney Diseases, Cystic/physiopathology ; Kidney Transplantation ; Living Donors ; Male ; Tissue and Organ Procurement/standards ; Tomography, X-Ray Computed/methods
    Language English
    Publishing date 2012-05
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 604539-x
    ISSN 1523-6838 ; 0272-6386
    ISSN (online) 1523-6838
    ISSN 0272-6386
    DOI 10.1053/j.ajkd.2012.02.002
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  4. Article ; Online: Bully renal cysts knock down urine-concentrating capacity in the early rounds.

    Grantham, Jared J

    Clinical journal of the American Society of Nephrology : CJASN

    2012  Volume 7, Issue 6, Page(s) 875–877

    MeSH term(s) Female ; Glycopeptides/blood ; Humans ; Kidney/physiopathology ; Kidney Concentrating Ability ; Male ; Neurophysins/blood ; Polycystic Kidney, Autosomal Dominant/blood ; Polycystic Kidney, Autosomal Dominant/physiopathology ; Protein Precursors/blood ; Vasopressins/blood
    Chemical Substances AVP protein, human ; Glycopeptides ; Neurophysins ; Protein Precursors ; copeptins ; Vasopressins (11000-17-2)
    Language English
    Publishing date 2012-06
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 2226665-3
    ISSN 1555-905X ; 1555-9041
    ISSN (online) 1555-905X
    ISSN 1555-9041
    DOI 10.2215/CJN.03720412
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Residual renal function: a paradigm shift.

    Lowenstein, Jerome / Grantham, Jared J

    Kidney international

    2017  Volume 91, Issue 3, Page(s) 561–565

    Abstract: Residual renal function (RRF) in patients undergoing dialysis treatments is currently viewed as glomerular filtrate that has escaped tubular reabsorption. RRF has been quantified as a clearance of urea or creatinine, or urea + creatinine. A major ... ...

    Abstract Residual renal function (RRF) in patients undergoing dialysis treatments is currently viewed as glomerular filtrate that has escaped tubular reabsorption. RRF has been quantified as a clearance of urea or creatinine, or urea + creatinine. A major paradigm shift has followed the recognition that a substantial number of organic anion retention solutes (possible "uremic toxins") are protein-bound and therefore are not readily filtered. These protein-bound aryl compounds are secreted by renal tubular organic anion transporters (OATs). This has led to the recognition that RRF in dialysis patients probably represents not only unreabsorbed glomerular filtrate but also a contribution of renal tubular transporters that secrete organic anions. Tubular secretion of hippurate, indoxyl sulfate, and p-cresol sulfate, protein-bound organic anions retained in the plasma of end-stage renal disease patients, can be quantified and used to evaluate the integrity of a function dependent on active solute transport. Here we propose a shift away from the exclusive "glomerulocentric" view of RRF as unreabsorbed glomerular filtrate and of the progression of renal disease as progressive glomerular loss. We expand the definition of RRF to include the combined renal and tubule functions remaining after a disease begins to destroy nephrons and proceeds to anuria. We propose renewed application of the first principles of renal physiology, articulated in the last century by Homer Smith, to the understanding and monitoring of RRF and progression of renal injury in patients during the sometimes long course of and at the end stage of chronic renal disease.
    MeSH term(s) Animals ; Disease Progression ; Glomerular Filtration Rate ; Humans ; Kidney Failure, Chronic/blood ; Kidney Failure, Chronic/physiopathology ; Kidney Failure, Chronic/therapy ; Kidney Glomerulus/metabolism ; Kidney Glomerulus/pathology ; Kidney Glomerulus/physiopathology ; Predictive Value of Tests ; Renal Dialysis/adverse effects ; Renal Insufficiency, Chronic/blood ; Renal Insufficiency, Chronic/diagnosis ; Renal Insufficiency, Chronic/physiopathology ; Renal Insufficiency, Chronic/therapy ; Terminology as Topic ; Toxins, Biological/blood ; Treatment Outcome ; Uremia/blood ; Uremia/diagnosis ; Uremia/physiopathology ; Uremia/therapy
    Chemical Substances Toxins, Biological
    Language English
    Publishing date 2017-03
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2016.09.052
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    Zs.A 797: Show issues Location:
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  6. Article ; Online: The rebirth of interest in renal tubular function.

    Lowenstein, Jerome / Grantham, Jared J

    American journal of physiology. Renal physiology

    2016  Volume 310, Issue 11, Page(s) F1351–5

    Abstract: The measurement of glomerular filtration rate by the clearance of inulin or creatinine has evolved over the past 50 years into an estimated value based solely on plasma creatinine concentration. We have examined some of the misconceptions and ... ...

    Abstract The measurement of glomerular filtration rate by the clearance of inulin or creatinine has evolved over the past 50 years into an estimated value based solely on plasma creatinine concentration. We have examined some of the misconceptions and misunderstandings of the classification of renal disease and its course, which have followed this evolution. Furthermore, renal plasma flow and tubular function, which in the past were estimated by the clearance of the exogenous aryl amine, para-aminohippurate, are no longer measured. Over the past decade, studies in experimental animals with reduced nephron mass and in patients with reduced renal function have identified small gut-derived, protein-bound uremic retention solutes ("uremic toxins") that are poorly filtered but are secreted into the lumen by organic anion transporters (OATs) in the proximal renal tubule. These are not effectively removed by conventional hemodialysis or peritoneal dialysis. Residual renal function, urine produced in patients with advanced renal failure or undergoing dialysis treatment, may represent, at least in part, secretion of fluid and uremic toxins, such as indoxyl sulfate, mediated by proximal tubule OATs and might serve as a useful survival function. In light of this new evidence of the physiological role of proximal tubule OATs, we suggest that measurement of renal tubular function and renal plasma flow may be of considerable value in understanding and managing chronic kidney disease. Data obtained in normal subjects indicate that renal plasma flow and renal tubular function might be measured by the clearance of the endogenous aryl amine, hippurate.
    MeSH term(s) Animals ; Glomerular Filtration Rate/physiology ; Humans ; Kidney Tubules/physiology ; Renal Dialysis
    Language English
    Publishing date 2016-06-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 603837-2
    ISSN 1522-1466 ; 0363-6127
    ISSN (online) 1522-1466
    ISSN 0363-6127
    DOI 10.1152/ajprenal.00055.2016
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  7. Article ; Online: The importance of total kidney volume in evaluating progression of polycystic kidney disease.

    Grantham, Jared J / Torres, Vicente E

    Nature reviews. Nephrology

    2016  Volume 12, Issue 11, Page(s) 667–677

    Abstract: The rate at which autosomal dominant polycystic kidney disease (ADPKD) progresses to end-stage renal disease varies widely and is determined by genetic and non-genetic factors. The ability to determine the prognosis of children and young adults with ... ...

    Abstract The rate at which autosomal dominant polycystic kidney disease (ADPKD) progresses to end-stage renal disease varies widely and is determined by genetic and non-genetic factors. The ability to determine the prognosis of children and young adults with ADPKD is important for the effective life-long management of the disease and to enable the efficacy of emerging therapies to be determined. Total kidney volume (TKV) reflects the sum volume of hundreds of individual cysts with potentially devastating effects on renal function. The sequential measurement of TKV has been advanced as a dynamic biomarker of disease progression, yet doubt remains among nephrologists and regulatory agencies as to its usefulness. Here, we review the mechanisms that lead to an increase in TKV in ADPKD, and examine the evidence supporting the conclusion that TKV provides a metric of disease progression that can be used to assess the efficacy of potential therapeutic regimens in children and adults with ADPKD. Moreover, we propose that TKV can be used to monitor treatment efficacy in patients with normal levels of renal function, before the pathologic processes of ADPKD cause extensive fibrosis and irreversible loss of functioning renal tissue.
    MeSH term(s) Disease Progression ; Humans ; Kidney/pathology ; Organ Size ; Polycystic Kidney Diseases/drug therapy ; Polycystic Kidney Diseases/etiology ; Polycystic Kidney Diseases/pathology ; Polycystic Kidney, Autosomal Dominant/pathology ; Prognosis ; Treatment Outcome
    Language English
    Publishing date 2016-10-03
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2490366-8
    ISSN 1759-507X ; 1759-5061
    ISSN (online) 1759-507X
    ISSN 1759-5061
    DOI 10.1038/nrneph.2016.135
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    Zs.A 6334: Show issues Location:
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    Zs.MG 107: Show issues

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  8. Book ; Conference proceedings: Problems in diagnosis and management of polycystic kidney disease

    Grantham, Jared J.

    proceed. of the First Internat. Workshop on Polycystic Kidney Disease [Sept. 29 - 30, 1984 ... held in Kansas City]

    1985  

    Title variant Polycystic kidney disease
    Event/congress International Workshop on Polycystic Kidney Disease (1, 1984, KansasCityMo.)
    Author's details Jared J. Grantham ... ed
    Keywords Kidney, Polycystic / congresses ; Zystenniere
    Subject Polyzystische Nierendegeneration ; Infantile Zystenniere ; Autosomal-dominante Zystenniere (Erwachsenenform)
    Size 264 S. : Ill., graph. Darst.
    Publisher PKR Foundation
    Publishing place Kansas City
    Publishing country United States
    Document type Book ; Conference proceedings
    HBZ-ID HT003201975
    ISBN 0-9614567-0-1 ; 978-0-9614567-0-2
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    1988 A 5011 order for loan Magazin

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  9. Article ; Online: Clinical practice. Autosomal dominant polycystic kidney disease.

    Grantham, Jared J

    The New England journal of medicine

    2008  Volume 359, Issue 14, Page(s) 1477–1485

    MeSH term(s) Adult ; Disease Progression ; Drinking ; Female ; Hematuria/etiology ; Humans ; Kidney/injuries ; Kidney Failure, Chronic/etiology ; Male ; Mutation ; Polycystic Kidney, Autosomal Dominant/diagnosis ; Polycystic Kidney, Autosomal Dominant/genetics ; Polycystic Kidney, Autosomal Dominant/therapy
    Language English
    Publishing date 2008-10-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMcp0804458
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  10. Article ; Online: Therapy for polycystic kidney disease? It's water, stupid!

    Grantham, Jared J

    Journal of the American Society of Nephrology : JASN

    2008  Volume 19, Issue 1, Page(s) 1–7

    MeSH term(s) Arginine Vasopressin/therapeutic use ; Humans ; Polycystic Kidney Diseases/drug therapy ; Polycystic Kidney Diseases/physiopathology ; Polycystic Kidney, Autosomal Dominant/drug therapy ; Polycystic Kidney, Autosomal Dominant/physiopathology ; Polycystic Kidney, Autosomal Recessive/drug therapy ; Polycystic Kidney, Autosomal Recessive/physiopathology ; Vasopressins/therapeutic use
    Chemical Substances Vasopressins (11000-17-2) ; Arginine Vasopressin (113-79-1)
    Language English
    Publishing date 2008-01
    Publishing country United States
    Document type Comment ; Editorial
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2007101100
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