DOCSLIB.ORG

Pediatric Nephrology

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Pediatric Nephrology Jennifer Leechik, RN, BSN, C(Neph)C Renal Nurse Clinician BC Children’s Hospital March 20, 2013 Outline the etiology of chronic kidney disease in the pediatric population Review common congenital and acquired disorders that lead to chronic kidney disease in the pediatric population Discuss diagnostic tools and treatments for pediatric patients Focus on concerns in the pediatric population Identify the different support systems in the pediatric population 2/3 of pediatric CKD is caused by acquired GN and congenital anomalies. About 15% of pediatric CKD is caused by rare hereditary diseases. Although diabetes and hypertension may begin in childhood, these disorders cause CKD about 5% of the time. Obstructive uropathy 19% Aplastic/hypoplastic/dysplastic kidney 18 Hereditary diseases 15 Focal segmental glomerulosclerosis 14 Reflux nephropathy 5 Chronic GN 4 Unknown 8 TOTAL 75% All other disease categories <4% each *North American Pediatric Renal Transplant Cooperative Study Glomerulonephritis/Vasculitis Focal segmental glomerulosclerosis (FSGS) Chronic GN, unclassifiable Hemolytic Uremic Syndrome (HUS) Idiopathic rapidly progressive GN (RPGN) Membranoproliferative GN (MPGN), Type I MPGN, Type II Lupus nephritis Henoch Schonlein purpura (HSP) IgA nephritis Membranous GN Other GN (Wegener’s, ANCA vasculitis) Commonly presented with Nephrotic Syndrome (NS) - proteinuria, hypoproteinemia, edema, hyperlipidemia Focal segmental glomerulosclerosis (FSGS) Membranoproliferative glomerulonephritis (MPGN) Type 1&2 Membranous Nephropathy - not usually with NS but with nephritis IgA Nephritis/ Nephropathy (Berger’s Disease) Lupus Nephritis Presentation with NS or proteinuria that is unresponsive or resistant to steroid therapy More likely to have hematuria and/or hypertension Less common cause of NS than minimal change disease in children < 10 years 50% reach CKD within 10 years If ESRD – 30% recurrence in initial transplant patients & >90% in subsequent transplants Presentation with NS, proteinuria or hematuria/nephritis that is controlled with steroid therapy Low serum C3 in >70% Type I progresses slowly to CKD in 10-20 years Type II often progresses rapidly Steroids: oral prednisone, 3 days of IV methylprednisolone Cytotoxic agents: cyclophosphamide, cyclosporine, mycofenilate mofetile (MMF) ACE Inhibitors/ARB Blockers: for chronic proteinuria Control hypertension and edema: fluid & sodium restriction Control anemia, renal osteodystrophy Commonly occurs in asian, african american and hispanic girls 80% of children with SLE have some kind of renal impairment Renal biopsy is needed for diagnosis and prognosis Focal (class III) or diffuse proliferative (class IV) nephritis & rarely membranous GN (class V) may progress to CKD Aggressively treating class III and IV with steroids or cytotoxic drugs is usually effective. Also known as “Hamburger Disease” Triad: Hemolytic anemia Uremia Thrombocytopenia Presentation with bloody diarrheal episodes, abdominal cramps, irritability, lethargy, fever and vomiting Peak age of onset: 1 – 2 years old Acute dialysis: 30% Chronic dialysis: ~5% E.Coli 0157 bacteria invades the GI tract and releases toxins that enter the bloodstream causing hemolysis of RBCs and platelets (cells become irregular and ‘sticky’) The damaged cells ‘clog’ the nephrons decreasing perfusion to the kidneys, decreasing u/o, causing electrolyte imbalances, increasing BP, etc. – Acute renal failure High risk of stroke, seizures, respiratory and cardiac issues No cure; only symptomatic management Vasculitis disorder that involves inflammation of the blood vessels Presents with: petechial and purpuric rash mainly to lower extremities Abdominal pain N/V; anorexia Arthralgias to lower joints with soft tissue edema Treatment: ◦ adequate hydration, or fluid intake ◦ careful attention to nutrition ◦ pain control with medications such as acetaminophen ◦ glucocorticoids (to control inflammation) Onset <20 yrs of age Aplasia/hypoplasia/dysplasia 44% Obstructive uropathy 40 Reflux nephropathy 12 Prune Belly Syndrome 4 Total 100% Aplasia: The absence of a kidney Usually unilateral If bilateral, associated with other defects such hypoplastic lungs, oligohydramnios Hypoplasia: Significantly small sized kidney with less nephrons; no dysplasia Unilateral or bilateral Usually develops hypertension Kidney malformation with differentiation of the metanephric tissue Unilateral or bilateral Usually small in size Maturation abnormality in the glomeruli and tubules More common than aplasia and hypoplasia Posterior Urethral Valves (PUV): ◦ Only in boys ◦ Valves situated at the distal portion of the prostatic urethra i.e. Proximal urethra causing obstruction in urine flow. ◦ Can be diagnosed antenatally during mother’s routine US that shows enlarged bladder, bilateral hydronephrosis, oligohydramnios. ◦ After birth, baby may have multiple UTIs and ‘dribbling’ ◦ Repair with ablation Ureteropelvic junction (UPJ) obstruction Uretovesical junction (UVJ) obstruction ◦ Less common Most common in caucasian girls Unilateral or bilateral Presents with multiple UTI Antibiotic prophylaxis may preserve function May develop CKD/ESRD as child grows older Familial – screen siblings Diagnosis by VCUG Renal U/S without (grades 1-2) or with (grades 3-5) hydronephrosis Also known as Eagle Barrett Syndrome Mostly in males Triad of symptoms: ◦ Complete or lack of abdominal muscle; wrinkled skin ◦ Undescended testicles ◦ Urinary tract abnormalities: Large ureter, large bladder, accumulation and backflow of urine Polycystic kidney disease 21% Medullary cystic/juvenile nephronophthisis 19 Congenital nephrotic syndrome 19 Familial nephritis (Alport) 16 Cystinosis 14 Denys-Drash/Fraser syndrome 4.5 Oxalosis (primary hyperoxaluria) 4 Sickle cell nephropathy 2 Other <1 Autosomal Recessive (“Infantile” PKD) enlarged kidneys found in fetus or at birth Tubular dilatation with small cysts in collecting ducts Associated with congenital hepatic fibrosis (scarring of the liver) – may need liver transplant ESRD usually before age 10 Autosomal Dominant (“Adult” PKD) Identifiable by multiple cysts on renal US in fetus, newborn or child, but usually diagnosed in adolescent or adult with hypertension Tubular dilatation with cysts throughout the nephron Cysts of liver, pancreas; Berry aneurysm of brain; diverticulosis ESRD usually after age 30 Medullary cystic disease Autosomal dominant Usually diagnosed in adolescence or adulthood Juvenile nephronophthisis Autosomal recessive Presents with polyuria, polydipsia, anemia, weakness, &/or growth failure in child <10y/o Often associated with other anomalies (skeletal, opthalmologic,developmental delay) Autosomal Recessive Finnish type: passed down through families Presents before 6 months of age Abnormal form of nephrin (protein) found in the kidneys Presents with cough, decrease u/o, foamy urine, failure to thrive, poor appetite, edema, hypertension Routine U/A shows large protein and fat. Treatment: ◦ Antibiotics to control infections ◦ Blood pressure meds: ACE inhibitors ◦ Albumin infusion (usually with diuretics) ◦ NSAIDS to slow protein buildup in the urine ◦ Possible nephrectomy and dialysis Prognosis: Can lead to death by 5 years of age but many die within their first year. Inherited disorder involving the basement membranes of the kidney, cochlea and the eye. 1) X-linked (80%) • Gene mutation • High sensory, progressive, sensorineural deafness • Lens abnormalities of the eyes • ESRD progression in mostly males by age of 20 2) Autosomal recessive (15%) • Deafness and ESRD for males and females by age of 30 3) Autosomal dominant (~5%) • Deafness and ESRD early in life • Associated thrombocytopenia and platelet abnormalities Metabolic disease Autosomal recessive Lysosomal storage disorder caused by defective transport of the amino acid cystine out of lysosomes that crystallizes damaging the tissues of kidneys and other organs. Fanconi Syndrome: proximal tubular wasting of amino acids, glucose, bicarb, phosphate, calcium, magnesium, uric acid, organic acids, low molecular wgt proteins, sodium, potassium and water Corneal ulcerations, retinal blindness, severe photophobia Severe growth failure; treated with GH Most common malignancy of the urinary tract in children Abnormal proliferation of metanephric blastema that develops nephrons 90% present before the age of 7 Peak onset at age 2-4 years old Treatment: Chemotherapy and/or radioactive therapy Resection of the tumor to preserve tissue > 85% survival rate with combination therapy Can lead to ESRD Need to be at least in remission for 1 year for kidney transplantation Specific therapy for specific disease Gene analysis Sibling/family screening Prenatal diagnosis ?Gene therapy in future Interstitial nephritis (IN) Idiopathic Can occur after streptococcal infection Drug related acute IN (methicillin, ampicillin, penicillin, sulfonamides, NSAIDS) Chronic pyelonephritis Associated with reflux nephropathy, chronic inflammation Not chronic urinary tract infection Presentation Mild proteinuria with few other urine abnormalities Hematuria in drug related cases Acute or chronic renal failure Blood work (urea, creatinine, electrolytes, hematology) Urine testing (U/A, C&S, 24hr) Ultrasound Cystoscopy, VCUG Renal biopsy Medication dosing are specific and ordered by the weight of the child. ◦ Oral: pills, capsules, liquid ◦ Intravenous, CVC ◦ NG/GT ◦ Intraperitoneal
Load more

Recommended publications
  • Hydronephrosis
    Hydronephrosis Natasha Brownrigg RN(EC), MN, NP-Pediatrics Assistant Clinical Professor, McMaster School of Nursing Nurse Practitioner, Pediatric Urology, McMaster Children’s Hospital, Hamilton, ON, Canada Dr. Jorge DeMaria Pediatric Urologist, McMaster Children’s Hospital Professor Department of Surgery/Urology, McMaster University, Hamilton, ON, Canada Dr. Luis H.P. Braga Pediatric Urologist, McMaster Children’s Hospital. Associate professor Department of Surgery/Urology, McMaster University, Hamilton, ON, Canada What is hydronephrosis? Hydro Nephrosis Hydronephrosis += Refers to water Refers to the kidney A build up of fluid or fluid (urine) in the kidney Hydronephrosis is the medical term for a build-up of urine in the kidney. As the urine builds up, it stretches or dilates the inside of the kidney, known as the collecting system. If an unborn baby has hydronephrosis, an ultrasound scan will show a build-up of urine in the kidney. This is called “antenatal hydronephrosis.” Hydronephrosis is found in as many as five out of 100 pregnancies. Hydronephrosis may also be found after birth. For example, if a baby has a urinary tract infection, an ultrasound of the baby’s kidneys and bladder may detect hydronephrosis. Key points to remember if your baby has hydronephrosis • Your baby can grow and develop normally with hydronephrosis. • Hydronephrosis may affect one kidney or both. • Hydronephrosis is a finding, not a disease. • Further tests are needed to find the cause of hydronephrosis. • If the cause is known, a pediatric urologist will discuss the possible treatment. Surgery is sometimes required to correct the cause of the hydronephrosis. Hydronephrosis is often transient and improves without any intervention.
    [Show full text]
  • Acute Phosphate Nephropathy Alexander K
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector http://www.kidney-international.org the renal consult & 2009 International Society of Nephrology Acute phosphate nephropathy Alexander K. Rocuts1, Sushrut S. Waikar1, Mariam P. Alexander1,2, Helmut G. Rennke2 and Ajay K. Singh1 1Renal Division, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA and 2Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts, USA minute. The rest of the examination was unremarkable. CASE PRESENTATION HerlaboratorydataissummarizedinTable1. A 60-year-old white Latino female with a clinical diagnosis A postoperative kidney ultrasound showed no of diabetes mellitus (diagnosed in 1993) and hypertension hydronephrosis. was referred to the chronic kidney disease clinic at The etiology of the acute kidney injury was unclear. Brigham and Women’s Hospital for the evaluation of acute Progressive diabetic nephropathy exacerbated by other kidney injury; serum creatinine had increased from a contributory factors, such as exposure to lisinopril, baseline of 0.9 to 1.5 mg/dl in a 11-week period. She was acetylsalicylic acid, or naproxen, was regarded as the most asymptomatic at the time of presentation. Her past plausible explanation. Despite discontinuation of these medical history included a total abdominal hysterectomy medications, kidney function did not improve; it worsened with bilateral salpingo oophorectomy and upper in a 4-week period after presentation. Hence, a kidney vaginectomy for high-grade squamous intraepithelial biopsy was performed. lesion of the cervix, 11 weeks prior to presentation. Three weeks prior to presentation (8 weeks after surgery) and within a week of each other, she was evaluated for two consecutive episodes of acute onset of chest pain with pulmonary edema in the setting of severe hypertension.
    [Show full text]
  • Annotations Prognosis for Vesicoureteric Reflux
    Arch Dis Child 1999;81:287–294 287 Arch Dis Child: first published as 10.1136/adc.81.4.287 on 1 October 1999. Downloaded from The Journal of the Royal College of Paediatrics and Child Health Annotations Prognosis for vesicoureteric reflux The prevalence of vesicoureteric reflux (VUR) has been to disentangle in this group of patients. The development estimated to be 2% of the child population.1 In children with of proteinuria is indicative of progressive glomerulosclero- VUR demonstrated on micturating cystourethrography sis and is a bad prognostic feature particularly when the there is a tendency for the grade of VUR to improve or for patient also has hypertension. VUR to disappear with time and with increasing age.23VUR has been identified as a risk factor for the development of Historical perspective urinary tract infections (UTI) and is present in a third of A review of literature in the preantibiotic era suggests that young children presenting with this problem. In addition, it chronic pyelonephritis was a very serious condition in chil- is a risk factor for renal scarring, otherwise called reflux dren and adults. Weiss and Parker described a series of nephropathy.45 VUR is also associated with renal dysplasia postmortem cases16: antecedent clinical features included and other developmental abnormalities of the urinary tract.6 recurrent fevers, presumably due to persistent untreated There is now abundant evidence for inheritance by an auto- infection, anaemia, hypertension, growth failure, and preg- somal dominant mechanism.7 nancy complications. There is evidence for a falling preva- lence of this condition, which is probably due to a true reduction of reflux nephropathy because of modern medi- Pathogenesis of reflux nephropathy cal care, particularly the treatment of acute pyelonephritis Studies have suggested that reflux nephropathy develops with antibiotics; alternatively the decline may represent following UTI in very early childhood or infancy.8 New changing fashions in disease classification.
    [Show full text]
  • Glomerulosclerosis in Reflux Nephropathy
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 21(1982), pp. 528—534 NEPHROLOGY FORUM Glomeruloscierosis in reflux nephropathy Principal discussant: RAMzI S. COTRAN Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts penis, testes, and urethral meatus were normal. The prostate was of normal size. Editors The BUN was 14 mg/dl; creatinine, 1.3 mg/dl (creatinine clearance, 113 mI/mm); blood chemistries were normal; the blood glucose was 93 JORDANJ. COHEN mg/dl; and the complement profile was normal. Serum protein was 7.5 JOHN 1. HARRINGTON gIdI with 4.3 g/dl albumin. Urinalysis showed a pH of 5; a specific JEROME P.KASSIRER gravity of 1.015; 4+ protein, no cells, and no bacteria. Urine culture was sterile. The 24-hour urine protein excretion was 2.4 g. Editor Chest x-ray showed borderline cardiomegaly with clear lungs. An Managing intravenous pyelogram revealed bilateral coarse scarring with caliecta- CHERYL J. ZUSMAN sis. The right kidney was smaller than the left. There was moderate ureterectasia extending down to the ureterovesical junction. A voiding cystourethrogram revealed a large-capacity bladder; the patient had no MichaelReese Hospital and Medical Center urge to void after almost 500 ml of contrast material was instilled. Bilateral reflux was greater and persistent on the left and was intermit- University of Chicago, tent on the right. The left ureter was dilated and tortuous. A left Pritzker School of Medicine ureterocele and right bladder diverticulum were visualized. and A biopsy of the left kidney showed focal scarring with interstitial New England Medical Center fibrosis and chronic inflammation, tubular atrophy, and dilation.
    [Show full text]
  • Predictors of Vesicoureteral Reflux in the Pretransplant Evaluation of Patients with End-Stage Renal Disease
    DOI: 10.14744/scie.2018.63935 Original Article South. Clin. Ist. Euras. 2018;29(3):176-179 Predictors of Vesicoureteral Reflux in the Pretransplant Evaluation of Patients with End-Stage Renal Disease Ergün Parmaksız, Meral Meşe, Zuhal Doğu, Zerrin Bicik Bahçebaşı ABSTRACT Objective: Voiding cystourethrography (VCUG) is widely performed in the pretransplant Department of Nephrology, evaluation of patients with a history of urological disorders to detect vesicoureteral reflux University of Health Sciences (VUR). The aim of this study was to evaluate the relationship between the primary etiology Kartal Dr. Lütfi Kırdar Training and Research Hospital, İstanbul, Turkey of end-stage renal disease (ESRD) and the prevalence of VUR, thereby determining the ne- cessity for VCUG in pretransplant patients. Submitted: 10.05.2018 Accepted: 27.08.2018 Methods: A total of 319 pretransplant cases that underwent VCUG were retrospectively reviewed. Correspondence: Ergün Parmaksız, SBÜ Kartal Dr. Lütfi Kırdar Results: VCUG revealed VUR in 53 (16.6%) cases. VUR was left-sided in 21 (41.2%), right- Eğitim ve Araştırma Hastanesi, Nefroloji Kliniği, İstanbul, Turkey sided in 18 (35.3%), and bilateral in 12 (3.8%), and grade 1 in 10 (19.6%), grade 2 in 19 E-mail: [email protected] (37.3%), grade 3 in 20 (39.2%), and grade 4 in 2 (3.9%). The etiology of ESRD was hyperten- sion in 125 (39.2%), diabetes mellitus (DM) in 46 (14.4%), polycystic kidney disease (PKD) in 21 (6.6%), amyloidosis in 16 (5%), VUR in 11 (3.4%), and glomerulonephritis (GN) in 11 (3.4%). The incidence of VUR was significantly higher in female patients.
    [Show full text]
  • Impact of Urolithiasis and Hydronephrosis on Acute Kidney Injury in Patients with Urinary Tract Infection
    bioRxiv preprint doi: https://doi.org/10.1101/2020.07.13.200337; this version posted July 13, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Impact of urolithiasis and hydronephrosis on acute kidney injury in patients with urinary tract infection Short title: Impact of urolithiasis and hydronephrosis on AKI in UTI Chih-Yen Hsiao1,2, Tsung-Hsien Chen1, Yi-Chien Lee3,4, Ming-Cheng Wang5,* 1Division of Nephrology, Department of Internal Medicine, Ditmanson Medical Foundation Chia-Yi Christian Hospital, Chia-Yi, Taiwan 2Department of Hospital and Health Care Administration, Chia Nan University of Pharmacy and Science, Tainan, Taiwan 3Department of Internal Medicine, Fu Jen Catholic University Hospital, Fu Jen Catholic University, New Taipei, Taiwan 4School of Medicine, College of Medicine, Fu Jen Catholic University, New Taipei, Taiwan 5Division of Nephrology, Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan *[email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/2020.07.13.200337; this version posted July 13, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. Abstract Background: Urolithiasis is a common cause of urinary tract obstruction and urinary tract infection (UTI). This study aimed to identify whether urolithiasis with or without hydronephrosis has an impact on acute kidney injury (AKI) in patients with UTI.
    [Show full text]
  • Renal Tubular Acidosis in Children: State of the Art, Diagnosis and Treatment
    www.medigraphic.org.mx Bol Med Hosp Infant Mex 2013;70(3):178-193 REVIEW ARTICLE Renal tubular acidosis in children: state of the art, diagnosis and treatment Ricardo Muñoz-Arizpe,1 Laura Escobar,2 Mara Medeiros3 ABSTRACT Overdiagnosis of renal tubular acidosis (RTA) has been recently detected in Mexican children, perhaps due to diagnostic errors as well as due to a lack of knowledge regarding the pathophysiology and molecular biochemistry involved in this illness. The objective of the present study is to facilitate the knowledge and diagnosis of RTA, a clinical condition infrequently seen worldwide. RTA is an alteration of the acid-base equilibrium due to a bicarbonate wasting in the proximal renal tubules [proximal RTA, (pRTA) or type 2 RTA] or due to a distal nephron hy- drogen ion excretion defect [distal RTA (dRTA) or type 1 RTA]. Hyperkalemic, or type 4 RTA, is due to alterations in aldosterone metabolism. RTA may be primary, secondary, acquired or hereditary and frequently presents secondary to an array of systemic diseases, usually accom- panied by multiple renal tubular defects. The main defect occurs in the transmembrane transporters such as carbonic anhydrase (CA I and + - - + - II), H -ATPase, HCO3 /Cl (AE1) exchanger and Na /HCO3 (NBCe1) cotransporter. Diagnosis should include the presence of hyperchloremic metabolic acidosis with normal serum anion gap (done in an arterial or arterialized blood sample), lack of appetite, polyuria, thirst, growth failure, and rickets; nephrocalcinosis and renal stones (in dRTA); abnormal urine anion gap and abnormal urine/serum pCO2 gradient. Diagnosis of a primary systemic disease must be made in cases of secondary RTA.
    [Show full text]
  • Silent Hydronephrosis, a Hazard Revisited
    SILENT HYDRONEPHROSIS, A HAZARD REVISITED By JOEL S. ROSEN, M.D., JOHN B. NANNINGA, M.D. and VINCENT J. O'CONOR, M.D. Midwest Regional Spinal Cord Injury Care System, Chicago, Illinois, U.S.A. Abstract. Six patients with neurogenic bladder secondary to spinal cord injury were seen in our Centre for routine follow-up. All of these individuals had attained the catheter-free state by various means and were, by their standards, functioning very well. They had gone from 6 months to 2t years without genito-urinary re-evaluations. One individual had a normal urogram I year after catheter removal and then 2 years later was noted to have bilateral hydronephrosis. Development of silent hydronephrosis in the catheter-free state, its treatment, and a regimen for following patients are discussed. THE recognition of hydronephrosis following spinal cord injury has been docu­ mented in the past by several authorities (Talbot & Bunts, 1940; Hutch & Bunts, 1951; Damanski & Gibbon, 1956). Damanski and Gibbon stated that hydro­ nephrosis occurred in one.;.third of a group of patients suffering from spinal cord injury. The changes have been reported to occur as early as 2 months after injury to as long as 8 years later. Ross (1963) has found hydronephrosis to be associated with the neural damage, urinary infection and back pressure; the importance of each factor varying considerably with the individual, Ascoli and Franch (1970) noted hydronephrosis most frequently in patients more than 4 years post trauma. Warning signs of impending hydronephrosis include the onset of urinary tract infection, deterioration of bladder function, increasing residual urine, bladder hypertonia and the appearance of bladder diverticula and reflux.
    [Show full text]
  • 2012 CKD Guideline
    OFFICIAL JOURNAL OF THE INTERNATIONAL SOCIETY OF NEPHROLOGY KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease VOLUME 3 | ISSUE 1 | JANUARY 2013 http://www.kidney-international.org KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease KDIGO gratefully acknowledges the following consortium of sponsors that make our initiatives possible: Abbott, Amgen, Bayer Schering Pharma, Belo Foundation, Bristol-Myers Squibb, Chugai Pharmaceutical, Coca-Cola Company, Dole Food Company, Fresenius Medical Care, Genzyme, Hoffmann-LaRoche, JC Penney, Kyowa Hakko Kirin, NATCO—The Organization for Transplant Professionals, NKF-Board of Directors, Novartis, Pharmacosmos, PUMC Pharmaceutical, Robert and Jane Cizik Foundation, Shire, Takeda Pharmaceutical, Transwestern Commercial Services, Vifor Pharma, and Wyeth. Sponsorship Statement: KDIGO is supported by a consortium of sponsors and no funding is accepted for the development of specific guidelines. http://www.kidney-international.org contents & 2013 KDIGO VOL 3 | ISSUE 1 | JANUARY (1) 2013 KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease v Tables and Figures vii KDIGO Board Members viii Reference Keys x CKD Nomenclature xi Conversion Factors & HbA1c Conversion xii Abbreviations and Acronyms 1 Notice 2 Foreword 3 Work Group Membership 4 Abstract 5 Summary of Recommendation Statements 15 Introduction: The case for updating and context 19 Chapter 1: Definition, and classification
    [Show full text]
  • A Veteran Presenting with Leg Swelling, Dyspnea, and Proteinuria Madeline Dilorenzo, MD; Jonathan X
    This PDF has been corrected to include a missing author. VA BOSTON MEDICAL FORUM A Veteran Presenting With Leg Swelling, Dyspnea, and Proteinuria Madeline DiLorenzo, MD; Jonathan X. Li, MD; Judith Strymish, MD; Jeffrey William, MD; and Anthony C. Breu, MD Madeline DiLorenzo Case Presentation. A 63-year-old male with well-controlled HIV (CD4 count 757, un- is a Resident in the Department of Internal detectable viral load), epilepsy, and hypertension presented to the VA Boston Health- Medicine at Boston care System (VABHS) emergency department with 1 week of bilateral leg swelling and University Medical exertional shortness of breath. He reported having no fever, cough, chest pain, pain with inspi- Center in Massachu- ration and orthopnea. There was no personal or family history of pulmonary embolism. He re- setts. Anthony Breu is a Hospitalist and the ported weight gain but was unable to quantify how much. He also reported flare up of chronic Director of Resident knee pain, without swelling for which he had taken up to 4 tablets of naproxen daily for sev- Education at VA Boston eral weeks. His physical examination was notable for a heart rate of 105 beats per minute and bi- Healthcare System and an Assistant Professor of lateral pitting edema to his knees. Laboratory testing revealed a creatinine level of 2.5 mg/dL, which Medicine at Harvard was increased from a baseline of 1.0 mg/dL (Table 1), and a urine protein-to-creatinine ratio of University in Massa- 7.8 mg/mg (Table 2). A renal ultrasound showed normal-sized kidneys without hydronephrosis or obstruct- chusetts.
    [Show full text]
  • Silent Hydronephrosis/Pyonephrosis Due to Upper Urinary Tract Calculi in Spinal Cord Injury Patients
    Spinal Cord (2000) 38, 661 ± 668 ã 2000 International Medical Society of Paraplegia All rights reserved 1362 ± 4393/00 $15.00 www.nature.com/sc Silent hydronephrosis/pyonephrosis due to upper urinary tract calculi in spinal cord injury patients S Vaidyanathan*,1, G Singh1, BM Soni1, P Hughes2, JWH Watt1, S Dundas3, P Sett1 and KF Parsons4 1Regional Spinal Injuries Centre, District General Hospital, Southport, Merseyside, UK; 2Department of Radiology, District General Hospital, Southport, Merseyside, UK; 3Department of Cellular Pathology, District General Hospital, Southport, Merseyside, UK; 4Department of Urology, Royal Liverpool University Hospital, Liverpool, UK Study design: A study of four patients with spinal cord injury (SCI) in whom a diagnosis of hydronephrosis or pyonephrosis was delayed since these patients did not manifest the traditional signs and symptoms. Objectives: To learn from these cases as to what steps should be taken to prevent any delay in the diagnosis and treatment of hydronephrosis/pyonephrosis in SCI patients. Setting: Regional Spinal Injuries Centre, Southport, UK. Methods: A retrospective review of cases of hydronephrosis or pyonephrosis due to renal/ ureteric calculus in SCI patients between 1994 and 1999, in whom there was a delay in diagnosis. Results: A T-5 paraplegic patient had two episodes of urinary tract infection (UTI) which were successfully treated with antibiotics. When he developed UTI again, an intravenous urography (IVU) was performed. The IVU revealed a non-visualised kidney and a renal pelvic calculus. In a T-6 paraplegic patient, the classical symptom of ¯ank pain was absent, and the symptoms of sweating and increased spasms were attributed to a syrinx.
    [Show full text]
  • Understanding Hydronephrosis, Fetal Medicine Program UCSF Benioff
    UCSF BENIOFF Children’S HOSPITAL OAKLAND UNDERSTANDING HYDRONEPHROSIS: PrenataL DIAGNOSIS Hydronephrosis Overview Hydronephrosis is dilation of the kidney, specifically the renal pelvis (place where urine is stored after its production). This can be the result of an anatomic abnormality in the urinary tract or can be a variant of normal. Hydronephrosis secondary to obstruction is typically at the level of the kidney (uretero-pelvic junction obstruction, or UPJ) or the bladder (uretero- Figure 1 vesical junction obstruction or megaureter). Please see Figure 1. How is Hydronephrosis What, if any, other test should be When should these diagnosed? done? tests be performed Hydronephrosis is usually • VCUG (voiding cystourethrogram): This study gives if a prenatal diagnosed in one of two ways. us important information regarding the shape and ultrasound showed 1. A prenatal ultrasound size of the bladder, the bladder neck (or opening) and hydronephrosis? (ultrasound during pregnancy) the tubes that drain the urine from the kidneys into If your newborn baby had may reveal a fetus with dilated the bladder, called ureters. It allows us to diagnose hydronephrosis (kidney, kidneys. This occurs in 1 per reflux (the abnormal back-flow of urine from the ureter, or bladder dilation) 100 pregnancies. bladder into the ureter and up to the kidney). It also noted on a screening pre- 2. An ultrasound done as a gives us additional anatomic information about the natal ultrasound, a repeat routine evaluation for another urethra (urine tube which takes urine from the bladder ultrasound should be medical problem, such as outside the body) to make sure no blockage is conducted in the first few a urinary tract infection or present (posterior urethral valves).
    [Show full text]