A Case of Pyonephrosis of an Obstructed Atrophic Kidney Fareeha Khan1,2*, Rasha Nakhleh3 and Theodore Suh1,2
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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. -
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. -
PATHOLOGY of the RENAL SYSTEM”, I Hope You Guys Like It
ﺑﺴﻢ اﷲ اﻟﺮﺣﻤﻦ اﻟﺮﺣﯿﻢ ھﺬه اﻟﻤﺬﻛﺮة ﻋﺒﺎرة ﻋﻦ إﻋﺎدة ﺗﻨﺴﯿﻖ وإﺿﺎﻓﺔ ﻧﻮﺗﺎت وﻣﻮاﺿﯿﻊ ﻟﻤﺬﻛﺮة زﻣﻼﺋﻨﺎ ﻣﻦ اﻟﺪﻓﻌﺔ اﻟﺴﺎﺑﻘﺔ ٤٢٧ اﻷﻋﺰاء.. ﻟﺘﺘﻮاﻓﻖ ﻣﻊ اﻟﻤﻨﮭﺞ اﻟﻤﻘﺮر ﻣﻦ اﻟﻘﺴﻢ ﺣﺮﺻﻨﺎ ﻓﯿﮭﺎ ﻋﻠﻰ إﻋﺎدة ﺻﯿﺎﻏﺔ ﻛﺜﯿﺮ ﻣﻦ اﻟﺠﻤﻞ ﻟﺘﻜﻮن ﺳﮭﻠﺔ اﻟﻔﮭﻢ وﺳﻠﺴﺔ إن ﺷﺎء اﷲ.. وﺿﻔﻨﺎ ﺑﻌﺾ اﻟﻨﻮﺗﺎت اﻟﻤﮭﻤﺔ وأﺿﻔﻨﺎ ﻣﻮاﺿﯿﻊ ﻣﻮﺟﻮدة ﺑﺎﻟـ curriculum ﺗﻌﺪﯾﻞ ٤٢٨ ﻋﻠﻰ اﻟﻤﺬﻛﺮة ﺑﻮاﺳﻄﺔ اﺧﻮاﻧﻜﻢ: ﻓﺎرس اﻟﻌﺒﺪي ﺑﻼل ﻣﺮوة ﻣﺤﻤﺪ اﻟﺼﻮﯾﺎن أﺣﻤﺪ اﻟﺴﯿﺪ ﺣﺴﻦ اﻟﻌﻨﺰي ﻧﺘﻤﻨﻰ ﻣﻨﮭﺎ اﻟﻔﺎﺋﺪة ﻗﺪر اﻟﻤﺴﺘﻄﺎع، وﻻ ﺗﻨﺴﻮﻧﺎ ﻣﻦ دﻋﻮاﺗﻜﻢ ! 2 After hours, or maybe days, of working hard, WE “THE PATHOLOGY TEAM” are proud to present “PATHOLOGY OF THE RENAL SYSTEM”, I hope you guys like it . Plz give us your prayers. Credits: 1st part = written by Assem “ THe AWesOme” KAlAnTAn revised by A.Z.K 2nd part = written by TMA revised by A.Z.K د.ﺧﺎﻟﺪ اﻟﻘﺮﻧﻲ 3rd part = written by Abo Malik revised by 4th part = written by A.Z.K revised by Assem “ THe AWesOme” KAlAnTAn 5th part = written by The Dude revised by TMA figures were provided by A.Z.K Page styling and figure embedding by: If u find any error, or u want to share any idea then plz, feel free to msg me [email protected] 3 Table of Contents Topic page THE NEPHROTIC SYNDROME 4 Minimal Change Disease 5 MEMBRANOUS GLOMERULONEPHRITIS 7 FOCAL SEGMENTAL GLOMERULOSCLEROSIS 9 MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS 11 DIABETIC NEPHROPATHY (new) 14 NEPHRITIC SYNDROME 18 Acute Post-infectious GN 19 IgA Nephropathy (Berger Disease) 20 Crescentic GN 22 Chronic GN 24 SLE Nephropathy (new) 26 Allograft rejection of the transplanted kidney (new) 27 Urinary Tract OBSTRUCTION, 28 RENAL STONES 23 HYDRONEPHROSIS -
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. -
RENAL BIOPSY and GLOMERULONEPHRITIS by J
Postgrad Med J: first published as 10.1136/pgmj.35.409.604 on 1 November 1959. Downloaded from 604 RENAL BIOPSY AND GLOMERULONEPHRITIS By J. H. Ross, M.D., M.R.C.P. Senior Medical Registrar, The Connaught Hospital, and Assistant, The Mledical Unit, The London Hospital Introduction sufficient to establish a diagnosis in a few condi- Safe methods of percutaneous renal biopsy were tions such as amyloid disease and diabetic first described by Perez Ara (1950) and Iversen glomerulosclerosis, but cortex with at least io and Brun (I95I) who used aspiration techniques. glomeruli is necessary for an accurate assessment Many different methods have since been described; of the renal structure; occasionally, up to 40 the simplest is that of Kark and Muehrcke (1954) glomeruli may be present in a single specimen. who use the Franklin modification of the Vim- The revelation of gross structural changes in Silverman needle. the kidneys of patients who can be recognized Brun and Raaschou (1958) have recently re- clinically as having chronic glomerulonephritis is viewed the majority of publications concerned of little value and does not contribute to manage- with renal biopsy and have concluded that the risk ment or prognosis. In contrast, biopsy specimensProtected by copyright. to the patients is slight. They mentioned three from patients in the early stages of glomerulo- fatalities which have been reported but considered nephritis, particularly those who have developed that, in each case, death was probably due to the the nephrotic syndrome insidiously without disease process rather than the investigation. haematuria or renal failure or who showy no Retroperitoneal haematomata have been recorded evidence of disease other than proteinuria, may in patients with hypertension or uraemia but are provide useful information. -
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. -
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. -
Guidelines on Urolithiasis
Guidelines on Urolithiasis C. Türk (chair), T. Knoll (vice-chair), A. Petrik, K. Sarica, A. Skolarikos, M. Straub, C. Seitz © European Association of Urology 2014 TABLE OF CONTENTS PAGE 1. METHODOLOGY 7 1.1 Introduction 7 1.2 Data identification 7 1.3 Evidence sources 7 1.4 Level of evidence and grade of recommendation 7 1.5 Publication history 8 1.5.2 Potential conflict of interest statement 8 1.6 References 8 2. CLASSIFICATION OF STONES 9 2.1 Stone size 9 2.2 Stone location 9 2.3 X-ray characteristics 9 2.4 Aetiology of stone formation 9 2.5 Stone composition 9 2.6 Risk groups for stone formation 10 2.7 References 11 3. DIAGNOSIS 12 3.1 Diagnostic imaging 12 3.1.1 Evaluation of patients with acute flank pain 12 3.1.2 Evaluation of patients for whom further treatment of renal stones is planned 13 3.1.3 References 13 3.2 Diagnostics - metabolism-related 14 3.2.1 Basic laboratory analysis - non-emergency urolithiasis patients 15 3.2.2 Analysis of stone composition 15 3.3 References 16 4. TREATMENT OF PATIENTS WITH RENAL COLIC 16 4.1 Renal colic 16 4.1.1 Pain relief 16 4.1.2 Prevention of recurrent renal colic 16 4.1.3 Recommendations for analgesia during renal colic 17 4.1.4 References 17 4.2 Management of sepsis in obstructed kidney 18 4.2.1 Decompression 18 4.2.2 Further measures 18 4.2.3 References 18 5. STONE RELIEF 19 5.1 Observation of ureteral stones 19 5.1.1 Stone-passage rates 19 5.2 Observation of kidney stones 19 5.3 Medical expulsive therapy (MET) 20 5.3.1 Medical agents 20 5.3.2 Factors affecting success of medical expulsive -
Guidelines on Urolithiasis
GUIDELINES ON UROLITHIASIS (Text update April 2010) Ch. Türk (chairman), T. Knoll (vice-chairman), A. Petrik, K. Sarica, C. Seitz, M. Straub, O. Traxer Eur Urol 2001 Oct;40(4):362-71 Eur Urol 2007 Dec;52(6):1610-31 J Urol 2007 Dec;178(6):2418-34 Methodology This update is based on the 2008 version of the Urolithiasis guidelines produced by the former guidelines panel. Literature searches were carried out in Medline and Embase for ran- domised control trials and systematic reviews published between January 1st, 2008, and November 30, 2009, and sig- nificant differences in diagnosis and treatment or in evidence level were considered. Introduction Urinary stone disease continues to occupy an important place in everyday urological practice. The average lifetime risk of stone formation has been reported in the range of 5-10%. Recurrent stone formation is a common problem with all types of stones and therefore an important part of the medical care of patients with stone disease. Classification and Risk Factors Different categories of stone formers can be identified based Urolithiasis 251 on the chemical composition of the stone and the severity of the disease (Table 1). Special attention must be given to those patients who are at high risk of recurrent stone formation (Table 2). Table 1: Categories of stone formers Stone composition Category Non-calcium Infection stones: INF stones Magnesium ammonium phosphate Ammonium urate Uric acid UR Sodium urate Cystine CY Calcium First time stone former, without residual So stones stone or stone fragments. First time stone former, with residual Sres stone or stone fragments. -
Path Renal Outline
Path Renal Outline Krane’s Categorization of Disease + A lot of Extras Kidney Disease Acute Renal Failure Intrinsic Kidney Disease Pre‐Renal Renal Intrinsic Post‐Renal Sodium Excretion <1% Glomerular Disease Tubulointerstitial Disease Sodium Excretion < 1% Sodium Excretion >2% Labs aren’t that useful BUN/Creatinine > 20 BUN/Creatinine < 10 CHF, Cirrhosis, Edema Urinalysis: Proteinuria + Hematuria Benign Proteinuria Spot Test Ratio >1.5, Spot Test Ratio <1.5, Acute Tubular Acute Interstitial Acute 24 Urine contains > 2.0g/24hrs 24 Urine contains < 1.0g/24hrs Necrosis Nephritis Glomerulonephritis Nephrotic Syndrome Nephritic Syndrome Inability to concentrate Urine RBC Casts Dirty Brown Casts Inability to secrete acid >3.5g protein / 24 hrs (huge proteinuria) Hematuria and Proteinuria (<3.5) Sodium Excretion >2% Edema Hypoalbuminemia RBC Casts Hypercholesterolemia Leukocytes Salt and Water Retention = HTN Focal Tubular Necrosis Edema Reduced GFR Pyelonephritis Minimal change disease Allergic Interstitial Nephritis Acute Proliferative Glomerulonephritis Membranous Glomerulopathy Analgesic Nephropathy Goodpasture’s (a form of RPGN) Focal segmental Glomerulosclerosis Rapidly Progressive Glomerulonephritis Multiple Myeloma Post‐Streptococcal Glomerulonephritis Membranoproliferative Glomerulonephritis IgA nephropathy (MPGN) Type 1 and Type 2 Alport’s Meleg‐Smith’s Hematuria Break Down Hematuria RBCs Only RBC + Crystals RBC + WBC RBC+ Protein Tumor Lithiasis (Stones) Infection Renal Syndrome Imaging Chemical Analysis Culture Renal Biopsy Calcium -
Factors in the Cause of Death in Carcinoma of the Cervix
FACTORS IN THE CAUSE OF DEATH IN CARCINOMA OF THE CERVIX A STUDY OF FIFTy-SEVEN CASES COMING TO NECROPSY B]ARNE PEARSON, M.D. (Prom the Cancer Institute and De;artment 01 Pathology, University of Minnesota Medkal School, Minneapolis ) This study is based upon 57 consecutive cases of carcinoma Qf the cervix in which autopsy examinations were performed. Thirty-one of these were studied at the University Hospitals. The remaining 26 were taken from the autopsy records in the Department of Pathology at the University of Minne sota. Microscopic sections were studied except in a few instances in which they could not be obtained. An attempt has been made to determine the im mediate lethal factors and the frequency with which they occur. No attempt is made to determine the efficacy of the treatment. URETERAL STRICTURE Stricture of the ureters with consequent hydronephrosis and hydroureters was the most striking and constant autopsy finding in this series of cases, being present in 42 cases, or 75 per cent. This is in accord with the observations of others. Ernst Holzbach in 4& carcinomas of the cervix coming to autopsy found 31 bilateral and 10 unilateral strictures. Sampson found that the fac tors responsible for strictures were external pressure of a mass of carcinoma around the ureters as a result of parametrial extension and lymphatic metasta sis, and added infection and edema. Carson states that metastasis may occur to the lymphatics of the ureters. Constriction by metastatic processes was not, however, very common in our series. It occurred only three times and was located in the midportion of the ureter. -
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