DOCSLIB.ORG

Renal Hemosiderosis Presenting with Acute Kidney Injury and Macroscopic Hematuria in Immunoglobulin a Nephropathy

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Renal Hemosiderosis Presenting with Acute Kidney Injury and Macroscopic Hematuria in Immunoglobulin a Nephropathy Taguchi et al. BMC Nephrology (2021) 22:132 https://doi.org/10.1186/s12882-021-02334-w CASE REPORT Open Access Renal hemosiderosis presenting with acute kidney Injury and macroscopic hematuria in Immunoglobulin A nephropathy: a case report Shinya Taguchi1,2*, Sumi Hidaka1, Mitsuru Yanai3,4, Kunihiro Ishioka1, Kenji Matsui1, Yasuhiro Mochida1, Hidekazu Moriya1, Takayasu Ohtake1 and Shuzo Kobayashi1 Abstract Background: Macroscopic hematuria-associated acute kidney injury (AKI) is a well-known complication of immunoglobulin A (IgA) nephropathy. In such cases, intratubular obstruction by red blood cell (RBC) casts and acute tubular necrosis are mainly observed pathologically. Herein, we report the case of a patient with IgA nephropathy presenting with AKI following an episode of macrohematuria. The patient presented with severe renal tubular hemosiderosis and acute tubular necrosis and without any obvious obstructive RBC casts. Case presentation: A 68-year-old woman, who was diagnosed with IgA nephropathy on renal biopsy 6 years ago, was admitted to our hospital after an episode of macroscopic glomerular hematuria and AKI following upper respiratory tract infection. Renal biopsy showed mesangial proliferation of the glomeruli, including crescent formation in 17 % of the glomeruli, and acute tubular necrosis without obvious hemorrhage or obstructive RBC casts. The application of Perls’ Prussian blue stain showed hemosiderin deposition in the renal proximal tubular cells. Immunofluorescence showed granular mesangial deposits of IgA and C3. Based on these findings, she was diagnosed with acute tubular necrosis with a concurrent IgA nephropathy flare-up. Moreover, direct tubular injury by heme and iron was considered to be the cause of AKI. She was treated with intravenous pulse methylprednisolone followed by oral prednisolone. Thereafter, the gross hematuria gradually faded, and her serum creatinine levels decreased. Conclusions: IgA nephropathy presenting with acute kidney injury accompanied by macrohematuria may cause renal hemosiderosis and acute tubular necrosis without obstructive RBC casts. Hemosiderosis may be a useful indicator for determining the pathophysiology of macroscopic hematuria-associated AKI. However, renal hemosiderosis may remain undiagnosed. Thus, Perls’ Prussian blue iron staining should be more widely used in patients presenting with hematuria. Keywords: IgA nephropathy, Macroscopic hematuria, Macrohematuria, Immunoglobulin A, Hemosiderin, Hemosiderosis, Acute kidney injury, Acute tubular necrosis * Correspondence: [email protected] 1Kidney Disease and Transplant Center, Shonan Kamakura General Hospital, 1370-1 Okamoto, 247-8553 Kamakura, Kanagawa, Japan 2Department of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, 236-0004 Yokohama, Japan Full list of author information is available at the end of the article © The Author(s). 2021 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. Taguchi et al. BMC Nephrology (2021) 22:132 Page 2 of 6 Background Table 1 Laboratory data on admission Macroscopic hematuria-associated acute kidney injury Parameter Value (reference range) (AKI) is a well-known complication of immunoglobulin A Hematology – (IgA) nephropathy (IgAN) [1 3]. In such cases, intratubu- White blood cell count, /µL 7400 (3000–9700) lar red blood cell (RBC) casts and acute tubular injury are Hemoglobin, mg/dL 12.6 (11.0–15.6) mainly observed pathologically [1–3].Additionally, depos- 4 – ition of hemosiderin in renal tubules has been reported in Platelet count, 10 /µL 29.7 (12.4 30.5) cases of paroxysmal nocturnal hemoglobinuria (PNH) [4] Blood chemistry and anticoagulant-related nephropathy (ARN) [5]present- Total protein, g/dL 7.4 (6.4–8.3) ing with AKI accompanied by macrohematuria. Herein, Albumin, g/dL 3.4 (3.8–5.2) we report the case of a patient with IgAN presenting with Urea nitrogen, mg/dL 62.1 (7.4–19.5) AKI accompanied by macrohematuria. The patient was Creatinine, mg/dL 4.92 (0.4–1.0) presented with severe renal tubular hemosiderosis and 2 acute tubular necrosis (ATN) without obvious obstructive eGFR, ml/min/1.73m 7.5 (> 60) RBC casts. In this case, renal hemosiderosis was expected AST, U/L 23 (12–35) to be the cause of the AKI. ALT, U/L 24 (6–40) LDH, U/L 229 (119–229) Case presentation FBS, mg/dL 143 (70–110) A 69-year-old woman was admitted to our hospital with a HbA1c, % 6.8 (4.6–6.2) 5-day history of macroscopic hematuria and AKI. She was – diagnosed with IgAN on renal biopsy 6 years prior. Fol- Triglyceride, mg/dL 169 (50 149) lowing this diagnosis, she was administered prednisolone LDL cholesterol, mg/dL 146 (70–139) because she had persistent microscopic hematuria and Immunology proteinuria of approximately 1.0 g/day. Proteinuria remit- IgG, mg/dL 1389 (820–1740) ted after treatment; however, microscopic hematuria per- IgA, mg/dL 736 (90–400) sisted (over 100 RBCs per high power field). Prednisolone IgM, mg/dL 67 (52–270) was discontinued 1 year ago. Five days prior to admission, – she developed an upper respiratory tract infection, accom- C3, mg/dL 157 (80 140) panied by gross hematuria. The gross hematuria persisted; C4, mg/dL 42 (11–34) however, the color became lighter after admission. Her CH50, U/mL 52 (30–45) past medical history included hypertension, diabetes, and C-reaction protein, mg/dL 6.31 (< 0.5) dyslipidemia. She was not receiving any antithrombotic Antinuclear antibody, IU/mL ×40 (< 40) medication. On admission, her body temperature, blood Anti-DNA antibody, IU/mL < 2.0 (0–6.0) pressure, and heart rate were 36.6℃, 144/64 mmHg, and – 65 beats/min, respectively. She had no abnormal findings MPO-ANCA, U/mL < 1.0 (0 3.5) on examination of her tonsils, pharynx, extremities, and PR3-ANCA, U/mL < 1.0 (0–3.5) skin. Laboratory data are presented in Table 1. Her serum ASO, IU/mL 50 (0–239) creatinine level increased to 4.9 mg/dl from 1.1 mg/dl at Urinalysis the last visit. Urinalysis revealed that the urinary protein Occult blood 3+ excretion level was 1.25 g/day; the sediments contained Dipstick protein 2+ 30–49 RBCs and ≥ 100 white blood cells per high-power – field. There were no signs of dehydration. Abdominal Red blood cell, /HPF 30 49 (< 5) ultrasound showed that both kidneys were of normal size, White blood cell, /HPF > 100 (< 5) excluding hydronephrosis. Protein urea, g/g creatinine 1.25 (< 0.15) A renal biopsy was performed 7 days after admission. Red blood cell cast (-) Light microscopy showed that nine out of 29 (31 %) eGFR estimated glomerular filtration rate; AST aspartate aminotransferase; glomeruli were globally sclerotic, and five out of 29 ALT alanine aminotransferase; LDH lactate dehydrogenase; FBS fasting blood (17 %) had cellular crescents. Most glomeruli showed sugar; HbA1c hemoglobin A1c; LDL low density lipoprotein; Ig immunoglobulin; MPO myeloperoxidase; PR3 proteinase 3; ANCA anti- moderate mesangial proliferation. The proximal tubule neutrophil cytoplasmic antibody; ASO anti-streptolysin epithelial cells were edematous, showed detachment from the tubular basement membrane, and contained obstructive RBC casts in the tubules. There was intersti- granules of various colors (ranging from yellow to tial fibrosis and inflammatory cells were present around brown). Some tubules showed dilation and loss of the the injured tubules (Fig. 1a–c). Immunofluorescence brush border. There was no obvious hemorrhage or showed granular mesangial staining for IgA and C3 Taguchi et al. BMC Nephrology (2021) 22:132 Page 3 of 6 Fig. 1 Microscopic findings of the renal biopsy. Periodic acid-Schiff staining shows tubular necrosis and pigments of various colors ranging from yellow to brown in the proximal tubular epithelial cells (a: ×400, b: ×400). a Black arrow shows loss of the brush border and swelling of the tubular epithelium. b Black arrow shows detachment of tubular epithelium from the basement membrane. Black arrowhead shows coagulative necrosis of the tubular epithelium. c Mesangial proliferation in the glomeruli (c: ×400). Immunofluorescence shows granular mesangial staining for immunoglobulin A (IgA) (d) and C3 (e), without staining for IgG, IgM, and C1q. Electron microscopy shows para-mesangial electron-dense deposits (f: ×8000, black arrow) (Fig. 1d, e). Electron microscopy showed mesangial RBC casts, which had never been reported previously. electron-dense deposits (Fig. 1 g). Perls’ Prussian blue This case suggests that hemosiderin-induced tubulotoxi- staining showed hemosiderin deposition in the renal city can be a major cause of AKI. proximal tubular cells, which was not observed 6 years In this case, there were no obvious obstructive RBC ago when first renal biopsy was performed (Fig. 2). Low casts in the tubules, which is commonly observed in vacuum scanning electron microscopy, a novel method patients with macroscopic hematuria-associated AKI [8]; for rapid three-dimensional pathological analysis [6, 7], however, significant hemosiderosis in the tubules was ob- showed the electron-dense particles in tubular epithelial served.
Load more

Recommended publications
  • Non-Commercial Use Only
    Veins and Lymphatics 2012; volume 1:e6 Ulcerated hemosiderinic three months previous to this therapy. Significant improvement in these injuries, Correspondence: Eugenio Brizzio and Alberto dyschromia and iron deposits with a reduction in the dimensions of the Lazarowski, San Martín 965, 1st floor (Zip code within lower limbs treated brown spot (9 of 9) at Day 90, and complete 1004) Buenos Aires, Argentina. with a topical application scarring with a closure time ranging from 15 Tel. +54.11.4311.5559. to 180 days (7 of 9) were observed. The use of E-mail: [email protected]; of biological chelator [email protected]; topical lactoferrin is a non-invasive therapeu- [email protected]; tic tool that favors clearance of hemosiderinic 1 2 [email protected] Eugenio Brizzio, Marcelo Castro, dyschromia and scarring of the ulcer. The 3 2 Marina Narbaitz, Natalia Borda, success of this study was not influenced Key words: ulcerated haemosiderinic dyschro- Claudio Carbia,2 Laura Correa,4 either by the hemochromatosis genetics or mia, liposomal Lactoferrin, scarring, hemo- Roberto Mengarelli,5 Amalia Merelli,2 the iron metabolism profile observed. siderin-ferritin. Valeria Brizzio,2 Maria Sosa,6 Acknowledgments: the authors would like to Biagio Biancardi,7 Alberto Lazarowski2 thank P. Girimonte for her assistance with the statistical analysis of the results. We also wish to Introduction thank the patients who made this study possible. 1International Group of Compression and Conference presentation: part of the present Argentina Medical Association, Buenos Chronic venous insufficiency (CVI) is one of study has been presented at the following con- 2 Aires, Argentina; Department of Clinical the most significant health problems in devel- gresses: i) XX Argentine Congress of Hematology, Biochemistry, Institute of oped countries.
    [Show full text]
  • Simple Technique to Identify Haemosiderin in Immunoperoxidase Stained Sections
    J Clin Pathol: first published as 10.1136/jcp.37.10.1190 on 1 October 1984. Downloaded from 1190 Technical methods Phosphate buffer at pH 8*0 gave the sharpest 2 Rozenszajn L, Leibovich M, Shoham D, Epstein J. The esterase staining reactions, although there was little differ- activity in megaloblasts, leukaemic and normal haemopoietic cells. Br J Haematol 1968; 14:605-19. ence at pH 7-0 or pH 7-5. As the buffer pH was 3Hayhoe FGJ, Quaglino D. Haematological cytochemistry. Edin- increased above pH 8-0 staining with both substrates burgh: Churchill Livingstone, 1980. became progressively weaker, especially above pH 4Li CY, Lam KW, Yam LT. Esterases in human leucocytes. J 9.0. Below pH 7-0 staining with a-naphthyl butyrate Histochem Cytochem 1973;21:1-12. Yam LT, Li CY, Crosby WH. Cytochemical identification of became weaker, and below pH 5*0 staining with monocytes and granulocytes. Am J Clin Pathol 1971;55:283- naphthol AS-D chloroacetate began to disappear. 90. 6 Armitage RJ, Linch DC, Worman CP, Cawley JC. The morphol- This work was supported by a Medical Research ogy and cytochemistry of human T-cell subpopulations defined by monoclonal antibodies and Fc receptors. Br J Haematol Council project grant. I thank Professor FGJ 1983;51:605-13. Hayhoe for valuable advice. References Requests for reprints to: Dr DM Swirsky, Department of Gomori G. Chloroacyl esters as histochemical substrates. J His- Haematological Medicine, University Clinical School, Hills tochem Cytochem 1953;1:469-70. Road, Cambridge CB2 2QL, England. Simple technique to identify identification of the two compounds on the same haemosiderin in slide.
    [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]
  • The Links Between Microbiome and Uremic Toxins in Acute Kidney Injury: Beyond Gut Feeling—A Systematic Review
    toxins Article The Links between Microbiome and Uremic Toxins in Acute Kidney Injury: Beyond Gut Feeling—A Systematic Review Alicja Rydzewska-Rosołowska 1,* , Natalia Sroka 1, Katarzyna Kakareko 1, Mariusz Rosołowski 2 , Edyta Zbroch 1 and Tomasz Hryszko 1 1 2nd Department of Nephrology and Hypertension with Dialysis Unit, Medical University of Białystok, 15-276 Białystok, Poland; [email protected] (N.S.); [email protected] (K.K.); [email protected] (E.Z.); [email protected] (T.H.) 2 Department of Gastroenterology and Internal Medicine, Medical University of Białystok, 15-276 Białystok, Poland; [email protected] * Correspondence: [email protected] Received: 30 October 2020; Accepted: 9 December 2020; Published: 11 December 2020 Abstract: The last years have brought an abundance of data on the existence of a gut-kidney axis and the importance of microbiome in kidney injury. Data on kidney-gut crosstalk suggest the possibility that microbiota alter renal inflammation; we therefore aimed to answer questions about the role of microbiome and gut-derived toxins in acute kidney injury. PubMed and Cochrane Library were searched from inception to October 10, 2020 for relevant studies with an additional search performed on ClinicalTrials.gov. We identified 33 eligible articles and one ongoing trial (21 original studies and 12 reviews/commentaries), which were included in this systematic review. Experimental studies prove the existence of a kidney-gut axis, focusing on the role of gut-derived uremic toxins and providing concepts that modification of the microbiota composition may result in better AKI outcomes. Small interventional studies in animal models and in humans show promising results, therefore, microbiome-targeted therapy for AKI treatment might be a promising possibility.
    [Show full text]
  • Urinary System Diseases and Disorders
    URINARY SYSTEM DISEASES AND DISORDERS BERRYHILL & CASHION HS1 2017-2018 - CYSTITIS INFLAMMATION OF THE BLADDER CAUSE=PATHOGENS ENTERING THE URINARY MEATUS CYSTITIS • MORE COMMON IN FEMALES DUE TO SHORT URETHRA • SYMPTOMS=FREQUENT URINATION, HEMATURIA, LOWER BACK PAIN, BLADDER SPASM, FEVER • TREATMENT=ANTIBIOTICS, INCREASE FLUID INTAKE GLOMERULONEPHRITIS • AKA NEPHRITIS • INFLAMMATION OF THE GLOMERULUS • CAN BE ACUTE OR CHRONIC ACUTE GLOMERULONEPHRITIS • USUALLY FOLLOWS A STREPTOCOCCAL INFECTION LIKE STREP THROAT, SCARLET FEVER, RHEUMATIC FEVER • SYMPTOMS=CHILLS, FEVER, FATIGUE, EDEMA, OLIGURIA, HEMATURIA, ALBUMINURIA ACUTE GLOMERULONEPHRITIS • TREATMENT=REST, SALT RESTRICTION, MAINTAIN FLUID & ELECTROLYTE BALANCE, ANTIPYRETICS, DIURETICS, ANTIBIOTICS • WITH TREATMENT, KIDNEY FUNCTION IS USUALLY RESTORED, & PROGNOSIS IS GOOD CHRONIC GLOMERULONEPHRITIS • REPEATED CASES OF ACUTE NEPHRITIS CAN CAUSE CHRONIC NEPHRITIS • PROGRESSIVE, CAUSES SCARRING & SCLEROSING OF GLOMERULI • EARLY SYMPTOMS=HEMATURIA, ALBUMINURIA, HTN • WITH DISEASE PROGRESSION MORE GLOMERULI ARE DESTROYED CHRONIC GLOMERULONEPHRITIS • LATER SYMPTOMS=EDEMA, FATIGUE, ANEMIA, HTN, ANOREXIA, WEIGHT LOSS, CHF, PYURIA, RENAL FAILURE, DEATH • TREATMENT=LOW NA DIET, ANTIHYPERTENSIVE MEDS, MAINTAIN FLUIDS & ELECTROLYTES, HEMODIALYSIS, KIDNEY TRANSPLANT WHEN BOTH KIDNEYS ARE SEVERELY DAMAGED PYELONEPHRITIS • INFLAMMATION OF THE KIDNEY & RENAL PELVIS • CAUSE=PYOGENIC (PUS-FORMING) BACTERIA • SYMPTOMS=CHILLS, FEVER, BACK PAIN, FATIGUE, DYSURIA, HEMATURIA, PYURIA • TREATMENT=ANTIBIOTICS,
    [Show full text]
  • Role of Urinalysis in the Diagnosis of Chronic Kidney Disease (CKD)
    Research and Reviews Role of Urinalysis in the Diagnosis of Chronic Kidney Disease (CKD) JMAJ 54(1): 27–30, 2011 Kunitoshi ISEKI*1 Abstract As of the end of Year 2008, 1 out of 450 people was a dialysis patient in Japan, and patients with chronic kidney disease (CKD) at stages 3 and 4 accounted for nearly 10% of the total population. An epidemiological study in Okinawa that used the introduction of dialysis treatment as the outcome revealed that the 10-year cumulative incident rate of end-stage renal disease (ESRD) was about 3% of the participants who were positive (Ն 1ϩ) for both proteinuria and hematuria, while there was hardly any difference between those who were positive for hematuria alone and those who were negative for both proteinuria and hematuria. When the incidence of ESRD (dialysis introduction) was examined in relation to the severity of proteinuria (5 grades ranging from [Ϫ] to [Ն 3ϩ]) as determined by dipstick, the cumulative incidence rate during the 17-year observation period was 16% for proteinuria (Ն 3ϩ) and about 7% for proteinuria (2ϩ). In contrast, among participants who were negative for proteinuria, the rate of dialysis introduction in 10 years is about 1 out of 1 million. The CKD Practice Guide of the Japanese Society of Nephrology recommends referral to a nephrologist when a case meets any of the following 3 criteria: 1) 0.5g/g creatinine or higher, or proteinuria (Ն 2ϩ), 2) an estimated glomerular filtration rate of less than 50ml/min/1.73m2, or 3) positive results (Ն 1ϩ) for both proteinuria and hematuria tests.
    [Show full text]
  • Renal Papillary Necrosis in Infancy PETER HUSBAND* and K
    Arch Dis Child: first published as 10.1136/adc.48.2.116 on 1 February 1973. Downloaded from Archives of Disease in Childhood, 1973, 48, 116. Renal papillary necrosis in infancy PETER HUSBAND* and K. A. HOWLETT From the Departments of Paediatrics and Radiology, Charing Cross Group of Hospitals, Fulham Hospital, London Husband, P., and Howlett, K. A. (1973). Archives of Disease in Childhood, 48, 116. Renal papillary necrosis in infancy. Two infants developed renal papillary necrosis after acute illnesses associated with dehydration. After a short oliguric phase there was a longer phase characterized by impaired urinary concen- tration, hyponatraemia, metabolic acidosis, and a raised blood urea. Intravenous urograms showed contrast collecting in the papillae, with subsequent sinus formation extending into the medulla. In one case impaired urinary concentration was still present 21 months after the initial illness. Renal papillary necrosis was originally described admitted to hospital 9 days later after he had been by Friedreich (1877) in a man aged 70 years. found in his cot, grey, with respiratory distress and a Since then the majority of further cases reported high temperature. 3 days before he had diarrhoea and have also been in adults. It has been thought to vomiting for 24 hours but subsequently tolerated feeds be uncommon and usually to have a fatal outcome of full cream Cow and Gate milk, 180 ml 5 times a day. He was again extremely ill: temperature 40 3 °C, pale, copyright. in infancy and childhood (Davies, Kennedy, and cyanosed with a rapid respiratory rate, but not dehydra- Roberts, 1969). In the newborn infant renal ted.
    [Show full text]
  • Risk of Renal Function Decline in Patients with Ketamine-Associated Uropathy
    International Journal of Environmental Research and Public Health Article Risk of Renal Function Decline in Patients with Ketamine-Associated Uropathy Shih-Hsiang Ou 1,2,3, Ling-Ying Wu 4, Hsin-Yu Chen 1,2, Chien-Wei Huang 1,2, Chih-Yang Hsu 1,2, Chien-Liang Chen 1,2 , Kang-Ju Chou 1,2, Hua-Chang Fang 1,2 and Po-Tsang Lee 1,2,* 1 Division of Nephrology, Department of Internal Medicine, Kaohsiung Veterans General Hospital, Kaohsiung 813, Taiwan; [email protected] (S.-H.O.); [email protected] (H.-Y.C.); [email protected] (C.-W.H.); [email protected] (C.-Y.H.); [email protected] (C.-L.C.); [email protected] (K.-J.C.); [email protected] (H.-C.F.) 2 Faculty of Medicine, School of Medicine, National Yang-Ming University, Taipei 112, Taiwan 3 Graduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan 4 Department of Obstetrics and Gynecology, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung 833, Taiwan; [email protected] * Correspondence: [email protected]; Tel.: +886-7342-2121 (ext. 8090) Received: 8 August 2020; Accepted: 29 September 2020; Published: 4 October 2020 Abstract: Ketamine-associated diseases have been increasing with the rise in ketamine abuse. Ketamine-associated uropathy is one of the most common complications. We investigated the effects of ketamine-associated uropathy on renal health and determined predictors of renal function decline in chronic ketamine abusers. This retrospective cohort study analyzed 51 patients (22 with ketamine- associated hydronephrosis and 29 with ketamine cystitis) from Kaohsiung Veterans General Hospital in Taiwan.
    [Show full text]
  • Hematuria in the Child
    Hematuria and Proteinuria in the Pediatric Patient Laurie Fouser, MD Pediatric Nephrology Swedish Pediatric Specialty Care Hematuria in the Child • Definition • ³ 1+ on dipstick on three urines over three weeks • 5 RBCs/hpf on three fresh urines over three weeks • Prevalence • 4-6% for microscopic hematuria on a single specimen in school age children • 0.3-0.5% on repeated specimens Sources of Hematuria • Glomerular or “Upper Tract” – Dysmorphic RBCs and RBC casts – Tea or cola colored urine – Proteinuria, WBC casts, renal tubular cells • Non-Glomerular or “Lower Tract” – RBCs have normal morphology – Clots/ Bright red or pink urine The Glomerular Capillary Wall The Glomerular Capillary Wall Glomerular Causes of Hematuria • Benign or self-limiting – Benign Familial Hematuria – Exercise-Induced Hematuria – Fever-Induced Hematuria Glomerular Causes of Hematuria • Acute Glomerular Disease – Poststreptococcal/ Postinfectious – Henoch-Schönlein Purpura – Sickle Cell Disease – Hemolytic Uremic Syndrome Glomerular Causes of Hematuria • Chronic Glomerular Disease – IgA Nephropathy – Henoch-Schönlein Purpura or other Vasculitis – Alport Syndrome – SLE or other Collagen Vascular Disease – Proliferative Glomerulonephritis Non-Glomerular Hematuria • Extra-Renal • UTI • Benign urethralgia +/- meatal stenosis • Calculus • Vesicoureteral Reflux, Hydronephrosis • Foreign body • Rhabdomyosarcoma • AV M • Coagulation disorder Non-Glomerular Hematuria • Intra-Renal • Hypercalciuria • Polycystic Kidney Disease • Reflux Nephropathy with Renal Dysplasia •
    [Show full text]
  • 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
    [Show full text]
  • Acute Tubular Necrosıs After Nephrectomy: Case Presentatıon
    Case Report JOJ Case Stud Volume 7 Issue 1 - May 2018 Copyright © All rights are reserved by Ebru Canakci DOI: 10.19080/JOJCS.2018.07.555703 Acute Tubular Necrosıs after Nephrectomy: Case Presentatıon Ebru Canakci1*, Ahmet Karatas2, Ahmet Gultekin1, Zubeyir Cebeci1, Ilker Coskun1 and Anıl Kılınc1 1Department of Anaesthesiology and Reanimation, Ordu University, Turkey 2Department of Internal Medicine & Nephrology, Ordu University, Turkey Submission: May 07, 2018; Published: May 18, 2018 *Corresponding author: Ebru Canakci, Faculty of Medicine, Department of Anaesthesiology and Reanimation, Ordu University, Ordu, Turkey, Email: Abstract ATN, contrary to prerenal azotemia, is not immediately cured upon the recovery of renal perfusion. In its severe form, renal hypoperfusion leads Acute renal failure (ARF) has a clinical presentation with declining renal function and glomerular filtration rate within hours-days. Ischemic trauma, severe hypovolemia, sepsis and severe burns. Acute kidney injury (AKI) is one of the frequently encountered causes of morbidity and mortalityto bilateral in renal hospitals. cortical The necrosis aim of this and study irreversible is to present renal the insufficiency. case with ATN Ischemic after major ATN often surgery develops and subsequent as a result permanent of major surgical kidney injuryintervention, in light of the information from the literature. Keywords: Nephrectomy; Acute Tubular Necrosis; Hemodialysis Introductıon and Objectıve to endogenous or exogenous toxins. Toxins cause intrarenal Acute renal failure (ARF) has a clinical presentation with vasoconstriction, direct tubular toxicity and/or intratubular obstruction and thus lead to ARF [4]. Acute kidney injury (AKI) hours-days. Although there are several differences in the declining renal function and glomerular filtration rate within is one of the frequently encountered causes of morbidity and mortality in hospitals.
    [Show full text]
  • Original Article Thrombocytopenia As a Predictor of Acute Kidney Injury in Patients with Emphysematous Pyelonephritis
    Int J Clin Exp Med 2019;12(1):849-854 www.ijcem.com /ISSN:1940-5901/IJCEM0078347 Original Article Thrombocytopenia as a predictor of acute kidney injury in patients with emphysematous pyelonephritis Heng Fan1,3*, Yu Zhao2*, Min Sun1, Jian-Hua Zhu1 1Department of Intensive Care Unit, Ningbo First Hospital, Ningbo, PR China; 2Department of Nephrology, Ningbo Urology and Nephrology Hospital, Ningbo, PR China; 3The Second School of Clinical Medicine, Southern Medical University, Guangzhou, PR China. *Equal contributors and co-first authors. Received April 22, 2018; Accepted September 12, 2018; Epub January 15, 2019; Published January 30, 2019 Abstract: Objective: The goal of this study was to investigate the relationship between thrombocytopenia and acute kidney injury (AKI) in patients with emphysematous pyelonephritis (EPN). Methods: A retrospective study was con- ducted in three university hospitals, and early hematological biomarkers were detected to predict the development of AKI in EPN patients. Results: Of 56 EPN patients, 32 (59%) developed AKI. Spearman correlation analysis showed that the nadir platelet count was negatively associated with the peak leukocyte count (r=-0.354, P<0.001), peak serum creatinine (r=-0.429, P<0.001), peak blood urea nitrogen (r=-0.317, P<0.001), and the length of hospital stay (r=-0.442, P<0.001). Furthermore, the area under the receiver-operating-characteristic curve (AU-ROC) was used to evaluate the accuracy of thrombocytopenia for the diagnosis of AKI in EPN patients, and the accuracy of nadir platelet count (AU-ROC: 0.92, 95% CI: 0.85-0.99, P<0.001) predicted AKI was significantly higher than admis- sion platelet count (AU-ROC: 0.84, 95% CI: 0.73-0.94, P<0.001).
    [Show full text]