DOCSLIB.ORG

Urinary Profiles

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Urinary Profiles URINARY PROFILES Giovanni B Fogazzi, MD, Milano, Italy Giuseppe Garigali, BSc, Milano, Italy Nuša Avguštin, MD, Ljubljiana, Slovenia THE FOUR PILLARS OF WISDOM OF URINARY MICROSCOPY 1. Sound laboratory methodology 2. Knowledge of all particles and their clinical meaning 3. Identification of the main urinary profiles (= combining urinary sediment findings with proteinuria and S-creatinine) 4. Placing of urinary findings into a wider laboratory and clinical context MAIN URINARY PROFILES • Isolated microscopic hematuria * • Glomerular diseases • Acute interstitial nephritis • Acute kidney injury • BK virus in kidney transplant recipients * • Urological disorders • Urinary tract infection * DEALT WITH IN OTHER PARTS OF THIS COURSE GLOMERULAR DISEASES A WIDE SPECTRUM OF URINARY PROFILES URINARY PROFILES IN GLOMERULAR DISEASES • Isolated dysmorphic microscopic hematuria • Isolated proteinuria • Proteinuria+microscopic hematuria • Gross hematuria (one shot,recurrent,persistent) • The nephritic sediment • The nephrotic sediment • The nephritic+nephrotic sediment S-CREATININE NORMAL OR INCREASED EITHER ACUTELY OR CHRONICALLY THE ACUTE NEPHRITIC SEDIMENT ACUTE NEPHRITIC SYNDROME DEFINITION: A condition characterised by the rapid increase of serum creatinine associated with hematuria (either microscopic or gross) and variable proteinuria,with/without high blood pressure CAUSES: Proliferative and/or necrotizing glomerulonephritis (GN), either primary or secondary PROLIFERATIVE GN GN characterised by increased numbers of cells (either local or from the circulation) within the glomeruli with/without necrotizing lesions PROLIFERATIVE GN IN OUR UNIT (in decreasing frequency) • IgA nephropathy • Paucimmune crescentic/necrotizing GN • Lupus nephritis (class III and IV) • Mesangiocapillary GN • Acute postinfectious • Schönlein-Henoch purpura GN A NORMAL GLOMERULUS IgA NEPHROPATHY Increased number of mesangial cells, increase of mesangial matrix and dominant IgA deposits) CRESCENTIC GN Crescents, either focal or diffuse, circumferential (A) or segmental ( B) A B THE NEPHRITIC SEDIMENT DISTINGUISHING PARTICLES: - RBCs (usually >50/HPF up to too many to count) - ERYTROCYTIC/hemoglobin CASTS ASSOCIATED PARTICLES: - WBCs (~1-10/HPF) - R-RTECs (0-≥≥≥1/HPF) - OTHER CASTS: epithelial, leukocytic, granular, waxy S-creatinine: rapid increase * Proteinuria: mild to ≥ 3.5 g/24 hours) THE NEPHRITIC SEDIMENT Many RBCs, often but not always dysmorphic THE NEPHRITIC SEDIMENT RBC casts ACUTE NEPHRITIC SEDIMENT: ORIGIN OF RBCs Bonsib SM. Am J Pathol 1985; 119:357-360 Scanning electron microscopy investigation on acellular glomeruli. Numerous holes and gaps of different size in the glomerular basement membrane of a patient with necrotizing (non proliferative) GN ACUTE NEPHRITIC SEDIMENT: ORIGIN OF WBCs Burkholder PM Am J Pathol 1969, 56: 251-265 Transmission electron microscopy investigation of glomerular basement membrane in acute proliferative GN. PMN passage through holes of GBM (arrows) SEQUENCE OF EVENTS LEADING TO NEPHRITIC SEDIMENT Glomerular Tubular epithelial proliferation ±±± necrosis damage RBC & WBC passage through gaps Detachment of tubular of GBM and their extravasation cells from tubular into Bowman’s space basement membrane RBC & WBC passage Tubular cells within into the tubular the tubular lumen lumen Tubular cells entrapment RBC & WBC entrapment within the matrix of casts within the matrix of casts forming in the tubules forming in the tubules Tubular cells and Hematuria RBC & WBC cylindruria epithelial casts Leukocyturia in the urine THE URINE SEDIMENT IN PROLIFERATIVE GNs The examination over time of the urine sediment is of particular importance in patients with chronic renal diseases which can recur after a phase of remission, such as lupus nephritis and small vessel vasculitis WHY? Together with other laboratory tests, the U-sed allows to evaluate whether the disease is quiescent rather than relapsing THE NEPHROTIC SEDIMENT THE NEPHROTIC SYNDROME DEFINITION: A condition characterized by proteinuria >3.5 g/24 hours, hypoalbuminemia, hypercholesterolemia and variable edema CAUSES: Non proliferative glomerular diseases, either primary or secondary NON PROLIFERATIVE GN GNs characterised by a normal number of cells within the glomerulus without necrotizing lesions NON PROLIFERATIVE GN IN OUR UNIT (in decreasing order) • Membranous nephropathy • Focal segmental glomerulosclerosis • Minimal change disease • Renal amyloidosis • Lupus nephritis (class V ) • Diabetic nephropathy A NORMAL GLOMERULUS MEMBRANOUS NEPHROPATHY Diffuse thickening of the glomerular basement mebranes associated with subepithelial/intramembranous deposits, mostly of IgG FOCAL SEGMENTAL GLOMERULOSCLEROSIS Areas of glomerular sclerosis with at times increased mesangial cellularity Sclerotic area DIABETIC NEPHROPATHY Diffuse mesangial expansion + sclerotic acellular nodules in the advanced phase Sclerotic acellular nodule THE NEPHROTIC SEDIMENT DISTINGUISHING PARTICLES: - No or few RBCs (usually not exceeding 20 to 30/HPF) - Fatty particles ASSOCIATED PARTICLES: - RTECs - CASTS: granular, fatty, epithelial (waxy in amyloidosis?) S-creatinine: normal to increased Proteinuria: >3.5 g/24 hours) URINARY LIPIDS IN NS • Fatty droplets (isolated or in clumps) • Oval fat bodies • Fatty casts • Cholesterol crystals LIPID DROPLETS OVAL FAT BODIES CHOLESTEROL FATTY CAST CRYSTAL MASSIVE LIPIDURIA MECHANISMS OF LIPIDURIA • Lipid ultrafiltration due to altered GBM permeability • Lipid reabsorption by proximal tubular cells • Intracellular transport into lysosomes • Active expulsion of lysosomes from the cells and tubular cellular detachment from tubular basement membrane LIPIDURIA IN PATIENTS WITH NEPHROTIC SYNDROME Ravignaux M-H et al Significance of cytolipiduria during a nephrotic syndrome Néphrologie 1991;12:12-16 NUMBER % WITH SEVERE LIPIDURIA (%) Membranoproliferative GN 12/15 80 5/12 (42) Amyloidosis 10/13 77 5/10 (50) Membranous nephropathy 18/25 72 10/18 (56) Focal segmental glomeruloscclerosis 14/22 64 14/22 (40) IgA nephropathy 4/7 57 1/4 (25) Intra-extracapillary GN 6/11 55 2/6 (33) Minimal change nephropathy 10/24 42 2/10 (20) FATTY PARTICLES IN GNs Fairley KF. Urinalysis. In: Diseases of the Kidney 5th Ed. Schrier RW and Gottschalk CW Eds. 1993, Boston, Little, Brown & Company, p 354 THE URINE SEDIMENT IN ACUTE INTERSTITIAL NEPHRITIS WHAT IS AIN? • It is a condition characterized by AKI associated with acute cellular infiltrate of the renal interstitium (mainly with lymphocytes, monocytes and plasma cells; less frequently also PMNs and/or eosinophils) • With possible extrarenal symptoms such as fever, skin rash, arthralgia, lumbar pain, etc • With different causes CAUSES OF AIN (Praga M & Gonzáles E. Kidney Int 2010; 77: 956-61) URINARY FINDINGS IN AIN COMMON VIEW ”A few and unspecific changes” Namely: • Low-grade tubular proteinuria (NOT detected by dipstick!!) * • Leukocyturia with/without eosinophiluria • Hematuria (either microscopic or macroscopic) * NSAIDs: glomerular proteinuria in nephrotic range EXPERTS VIEW (1) (Praga M & Gonzáles E. Kidney Int 2010; 77: 956-61) “Microscopic hematuria…is found in almost two-thirds of the patients, although the presence of red blood cell casts is rare . A very common finding (>80% of cases) is leukocyturia, frequently accompanied by leukocyte casts.” EXPERTS VIEW (2) (Perazella MA & Markowitz GS. Nat Rev Nephrol 2010;6:461) URINE SEDIMENT FINDINGS IN THE LITERATURE (BIOPSY-PROVEN CASES) * • Patient number 318 • RBCs 171 (53.7%) • WBCs 211 (66.3%) • RTECs --- • Casts 27 (8.5%) -granular 13 (4.0%) -undefined 10 (3.1%) -”cellular” 2 (0.6%) -leukocytic 1 (0.3%) -erythrocytic 1 (0.3%) *23 papers, from 1975 to 2010, selected because of adequate information on U-sed (drug-induced 17; general 6, including 2 pediatric series ) RBC CASTS IN THE URINE-1 Nine patients with biopsy-proven drug associated AIN. RBC casts found in the urine sediment of a 19-year-old man (11.1%) with AIN due to penicillin RBC CASTS IN THE URINE-2 Red Blood Cell Casts In Acute Interstitial Nephritis Jerald F. Sigala, MD; Claude G.Biava, MD; Henry N. Hulter, MD Arch Intern Med 138: 1419-1421, 1978 “A 45-year-old woman receiving hydralazine and hydrochlorothiazide therapy was found to have a reduced glomerular filtration rate, a positive antinuclear antibody reaction, and RBC casts in the urinary sediment . Glomeruli with normal morphology were found on renal biopsy; however a mild interstitial nephritis was observed that predominantly involved the distal tubules…..” “Although RBC casts have been thought to be diagnostic of glomerular diseases, the present case demonstrates that tubulointerstitial disease can be responsible for RBC cast formation.” RBC CASTS IN THE URINE-3 RBC casts in the urine sediment of 4 out of 12 patients with unspecified AIN (33.3%). Neither details nor comments found in the paper AIN: OUR RETROSPECTIVE EXPERIENCE (1997-2010) Number 21 (biopsy-proven) M:F 12:9 Age 55.4 ±±± 19.6 (17-80) S-creatinine at RB 4.5 ±±± 3.2 (1.4-14.6) Proteinuria 19/21 (90.4%) (g/24hrs) 1.3 ±±± 2.7 (0.2-12.1) 7 NSAID Cause 5 Antibiotics 4 Unidentified 3 Salazopyrin 2 Other (PPI: 1; Doxazosin 1) URINE SEDIMENT FINDINGS (1) U-sed PARTICLE OUR COHORT (21) LITERATURE (318) WBCs 12 (57.1%) 211 (66.3%) RBCs 10 (47.6%) 171 (53.7%) RTECs 3 (14.2%) --- CASTS 20 (95.2%) 27 (8.5%) Hyaline 19 (90.4%) --- Hyaline-granular 17 (80.9%) --- Granular 13 (61.9%) 13 (4.0%) Waxy 0 --- Erythrocytic 6 (28.5%) 1 (0.3%) Epithelial (RTECs) 3 (14.2%) --- Leukocytic 3 (14.2%) 1 (0.3%) URINE SEDIMENT
Load more

Recommended publications
  • A Dipstick Test Combined with Urine Specific Gravity Improved the Accuracy of Proteinuria Determination in Pregnancy Screening
    Kobe J. Med. Sci., Vol. 56, No. 4, pp. E165-E172, 2010 A Dipstick Test Combined with Urine Specific Gravity Improved the Accuracy of Proteinuria Determination in Pregnancy Screening NATSUKO MAKIHARA1, MINEO YAMASAKI1,2, HIROKI MORITA1, and HIDETO YAMADA1* 1Division of Obstetrics and Gynecology, Department of Surgery-related, and 2Division of Integrated Medical Education, Department of Community Medicine and Social Healthcare Science, Kobe University Graduate School of Medicine, 7-5-1 Kusunoki-cho, Chuo-ku, Kobe, 650-0017, Japan. Received 12 July 2010/ Accepted 20 August 2010 Key Words: dipstick test, pregnancy proteinuria, protein/creatinine ratio, urine specific gravity Proteinuria screening using a semi-quantitative dipstick test of the spot urine in antenatal clinic is known to have high false-positive rates. The aim of this study was to assess availability of a dipstick test combined with the urine specific gravity for the determination of pathological proteinuria. A dipstick test was performed on 582 urine samples obtained from 283 pregnant women comprising 260 with normal blood pressure and 23 with pregnancy-induced hypertension. The urine protein (P) and creatinine (C) concentrations, specific gravity (SG), P/C ratio were determined, and compared with dipstick test results. The P concentration increased along the stepwise augmentations in dipstick test result. Frequencies of the urine samples with 0.265 or more P/C ratio were 0.7% with − dipstick test result, 0.7% with the ± result, 3.3% with the 1+ result, and 88.9% with the ≥2+ result. However, if the urine specific gravity was low, frequencies of the high P/C ratio were 5.0% with ± dipstick test result and 9.3% with the 1+ result.
    [Show full text]
  • Proteinuria and Albuminuria: What’S the Difference? Cynthia A
    EXPERTQ&A Proteinuria and Albuminuria: What’s the Difference? Cynthia A. Smith, DNP, CNN-NP, FNP-BC, APRN, FNKF What exactly is the difference between TABLE Q the protein-to-creatinine ratio and the Persistent Albuminuria Categories microalbumin in the lab report? How do they compare? Category Description UACR For the non-nephrology provider, the options for A1 Normal to mildly < 30 mg/g evaluating urine protein or albumin can seem con- increased (< 3 mg/mmol) fusing. The first thing to understand is the impor- tance of assessing for proteinuria, an established A2 Moderately 30-300 mg/g marker for chronic kidney disease (CKD). Higher increased (3-30 mg/mmol) protein levels are associated with more rapid pro- A3 Severely > 300 mg/g gression of CKD to end-stage renal disease and in- increased (> 30 mg/mmol) creased risk for cardiovascular events and mortality in both the nondiabetic and diabetic populations. Abbreviation: UACR, urine albumin-to-creatinine ratio. Monitoring proteinuria levels can also aid in evaluat- Source: KDIGO. Kidney Int. 2012.1 ing response to treatment.1 Proteinuria and albuminuria are not the same low-up testing. While the UACR is typically reported thing. Proteinuria indicates an elevated presence as mg/g, it can also be reported in mg/mmol.1 Other of protein in the urine (normal excretion should be options include the spot urine protein-to-creatinine < 150 mg/d), while albuminuria is defined as an “ab- ratio (UPCR) and a manual reading of a reagent strip normal loss of albumin in the urine.”1 Albumin is a (urine dipstick test) for total protein.
    [Show full text]
  • Understanding What It Means to Have Protein in Your Urine Understanding What It Means to Have Protein in Your Urine
    UNDERSTANDINGUnderstanding WHAT ITYour MEANS TO HAVE Hemodialysis PROTEINAccess Options IN YOUR URINE 2 AAKP: Understanding What It Means to Have Protein in Your Urine Understanding What It Means to Have Protein in Your Urine The kidneys are best known for making urine. This rather simple description does not tell the whole story. This brochure describes other important functions of the kidneys; including keeping protein in the blood and not letting any of the protein in the liquid (plasma) part of blood escape into the urine. Proteinuria is when “Proteinuria” is when kidneys allow proteins to kidneys appear in the urine and be lost from the body. allow Proteinuria is almost never normal, but it can proteins to be normal - rarely - in some healthy, active appear in the urine children or young adults. and be The kidneys are paired organs located on either lost from the body. side of the backbone. They are located at the Proteinuria level of the lowest part of the rib cage. They are is almost the size of an adult fist (4.5 – 5 inches in length). never Together the two kidneys receive a quarter of normal, but it can the blood that is pumped from the heart every be normal minute. This large blood flow is needed in order - rarely - for the kidneys to do one of the kidneys’ main in some jobs: healthy, active • remove waste products in the blood every children day or young adults. • keep the body in balance by eliminating the extra fluids and salts we consume on a regular basis.
    [Show full text]
  • Storm in a Pee Cup: Hematuria and Proteinuria
    Storm in a Pee Cup: Hematuria and Proteinuria Sudha Garimella MD Pediatric Nephrology, Children's Hospital-Upstate Greenville SC Conflict of Interest • I have no financial conflict of interest to disclose concerning this presentation. Objectives • Interpret the current guidelines for screening urinalysis, and when to obtain a urinalysis in the pediatric office. • Interpret the evaluation of asymptomatic/isolated proteinuria and definitions of abnormal ranges. • Explain the evaluation and differential diagnosis of microscopic hematuria. • Explain the evaluation and differential diagnosis of gross hematuria. • Explain and discuss appropriate referral patterns for hematuria. • Racial disparities in nephrology care 1. APOL-1 gene preponderance in African Americans and risk of proteinuria /progression(FSGS) 2. Race based GFR calculations which have caused harm 3. ACEI/ARB usage in AA populations: myths and reality Nephrology Problems in the Office • Hypertension • Proteinuria • Microscopic Hematuria • Abnormal Renal function The Screening Urinalysis • Choosing Wisely: • Don’t order routine screening urine analyses (UA) in healthy, asymptomatic pediatric patients as part of routine well child care. • One study showed that the calculated false positive/transient abnormality rate approaches 84%. • Population that deserves screening UA: • patients who are at high risk for chronic kidney disease (CKD), including but not necessarily limited to patients with a personal history of CKD, acute kidney injury (AKI), congenital anomalies of the urinary tract, acute nephritis, hypertension (HTN), active systemic disease, prematurity, intrauterine growth retardation, or a family history of genetic renal disease. • https://www.choosingwisely.org/societies/american-academy-of-pediatrics-section-on- nephrology-and-the-american-society-of-pediatric-nephrology/ Screening Urinalysis: Components A positive test for leukocyte esterase may be seen in genitourinary inflammation, irritation from instrumentation or catheterization, glomerulonephritis, UTIs and sexually transmitted infections.
    [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]
  • Article Utility of Urine Eosinophils in the Diagnosis of Acute Interstitial
    Article Utility of Urine Eosinophils in the Diagnosis of Acute Interstitial Nephritis Angela K. Muriithi,* Samih H. Nasr,† and Nelson Leung* Summary Background and objectives Urine eosinophils (UEs) have been shown to correlate with acute interstitial nephritis (AIN) but the four largest series that investigated the test characteristics did not use kidney biopsy as the gold standard. *Division of Nephrology and Hypertension, Design, setting, participants, & measurements This is a retrospective study of adult patients with biopsy-proven Department of diagnoses and UE tests performed from 1994 to 2011. UEs were tested using Hansel’s stain. Both 1% and 5% UE Internal Medicine, cutoffs were compared. Mayo Clinic, Rochester, Minnesota; and †Department of Results This study identified 566 patients with both a UE test and a native kidney biopsy performed within a week Laboratory Medicine of each other. Of these patients, 322 were men and the mean age was 59 years. There were 467 patients with and Pathology. Mayo pyuria, defined as at least one white cell per high-power field. There were 91 patients with AIN (80% was drug Clinic, Rochester, induced). A variety of kidney diseases had UEs. Using a 1% UE cutoff, the comparison of all patients with AIN to Minnesota those with all other diagnoses showed 30.8% sensitivity and 68.2% specificity, giving positive and negative ’ Correspondence: likelihood ratios of 0.97 and 1.01, respectively. Given this study s 16% prevalence of AIN, the positive and Dr. Angela K. Muriithi, negative predictive values were 15.6% and 83.7%, respectively. At the 5% UE cutoff, sensitivity declined, but Mayo Clinic, Division specificity improved.
    [Show full text]
  • Blood Or Protein in the Urine: How Much of a Work up Is Needed?
    Blood or Protein in the Urine: How much of a work up is needed? Diego H. Aviles, M.D. Disclosure • In the past 12 months, I have not had a significant financial interest or other relationship with the manufacturers of the products or providers of the services discussed in my presentation • This presentation will not include discussion of pharmaceuticals or devices that have not been approved by the FDA Screening Urinalysis • Since 2007, the AAP no longer recommends to perform screening urine dipstick • Testing based on risk factors might be a more effective strategy • Many practices continue to order screening urine dipsticks Outline • Hematuria – Definition – Causes – Evaluation • Proteinuria – Definition – Causes – Evaluation • Cases You are about to leave when… • 10 year old female seen for 3 day history URI symptoms and fever. Urine dipstick showed 2+ for blood and no protein. Questions? • What is the etiology for the hematuria? • What kind of evaluation should be pursued? • Is this an indication of a serious renal condition? • When to refer to a Pediatric Nephrologist? Hematuria: Definition • Dipstick > 1+ (large variability) – RBC vs. free Hgb – RBC lysis common • > 5 RBC/hpf in centrifuged urine • Can be – Microscopic – Macroscopic Hematuria: Epidemiology • Microscopic hematuria occurs 4-6% with single urine evaluation • 0.1-0.5% of school children with repeated testing • Gross hematuria occurs in 1/1300 Localization of Hematuria • Kidney – Brown or coke-colored urine – Cellular casts • Lower tract – Terminal gross hematuria – (Blood
    [Show full text]
  • A Complicated Case of Von Hippel-Lindau Disease
    Postgrad Med J 2001;77:471–480 471 Postgrad Med J: first published as 10.1136/pmj.77.909.478 on 1 July 2001. Downloaded from SELF ASSESSMENT QUESTIONS A complicated case of von Hippel-Lindau disease G Thomas, R Hillson Answers on p 481. A 17 year old female shop assistant presented with a three week history of generalised headache, associated with nausea, vomiting, and vertigo. She had no past medical history, and was taking no regular medication. Her mother was currently receiving radiotherapy for anaplastic carcinoma of the thyroid gland. On examination she had an ataxic gait, bilateral papilloedema, and horizontal nystagmus to right lateral gaze. Left sided dysdiadokinesis and hyper-reflexia were demonstrated. Power and sensation were preserved. Computed tom- ography of the brain revealed a cystic lesion within the left cerebellum. Subsequent mag- netic resonance imaging (MRI) revealed a sec- ond, non-cystic lesion within the region of the right vermis (fig 1). Both images were consist- ent with cerebellar haemangioblastomata. A posterior fossa craniotomy was performed, with successful excision of both tumours. She made an uneventful recovery, with complete resolution of all symptoms, and was subse- Figure 3 MIBG isotope quently discharged. uptake scan. During a follow up outpatient appointment Figure 1 MRI of the brain. six months later, she complained of frequent panic attacks, associated with sweating and http://pmj.bmj.com/ palpitation that had begun two months earlier. These episodes were precipitated by exercise or excitement. She gave no history of heat intoler- Department of ance, weight loss, or diarrhoea. Examination Diabetes and was entirely normal.
    [Show full text]
  • Eosinophiluria in Relation to Pyelonephritis in Women
    Journal of Advanced Laboratory Research in Biology E-ISSN: 0976-7614 Volume 6, Issue 4, 2015 PP 108-110 https://e-journal.sospublication.co.in Research Article Eosinophiluria in relation to Pyelonephritis in Women Pritam Singh Ajmani* Department of Pathology, R.D. Gardi Medical College, Surasa, Ujjain, Madhya Pradesh-456006, India. Abstract: In the present study of outpatient settings, pyelonephritis was diagnosed by the history and physical examination and supported by urinalysis results. After a clinco-pathological confirmation of pyelonephritis in 100 female patients in the age group between 18-55 years were selected. The urine samples were subjected for routine urine analysis and urine sediment was stained with Wright-Giemsa stain. A total of 13% of these patients had eosinophils in urine. Eosinophiluria is defined as the presence of more than 1% eosinophils in urinary sediment under the microscope. Eosinophiluria proved to be good predictors of pyelonephritis, however, it is not specific. Positive test for pyuria of moderate to severe were seen in all (100%) of the cases. Microscopic hematuria was seen in 18% cases. We have found that Wright-Giemsa stain results show consistent results and eosinophils were more easily recognized. Demographic data collected were age, weight, gravidity, and parity. The gestational age of diagnosis was recorded. Keywords: Urine, Wright-Giemsa Stain, Eosinophiluria. 1. Introduction 3. Microscopic Pyuria. 4. Gross Hematuria. Pyelonephritis is a common bacterial infection of 5. Microscopic Hematuria. the renal pelvis and kidney that usually results from 6. WBC casts Indicative of renal origin. ascent of a bacterial pathogen up the ureters from the 7.
    [Show full text]
  • USMLE and COMLEX II
    USMLE and COMLEX Review Nephrology Supplement Glomerulonephritis, Acute Tubular Necrosis and Acute Interstitial Nephritis Northwestern Medical Review www.northwesternmedicalreview.com Lansing, Michigan 2014-2015 1. What is Tamm-Horsfall glycoprotein (THP)? Matching (4 – 15): Match the following urinary casts with the descriptions, conditions, or questions _______________________________________ presented hereafter: _______________________________________ A. Bacterial casts _______________________________________ B. Crystal casts _______________________________________ C. Epithelial casts D. Fatty casts _______________________________________ E. Granular casts _______________________________________ F. Hyaline casts G. Pigment casts H. Red blood cell casts 2. What is a urinary cast? I. Waxy casts J. White blood cell casts _______________________________________ _______________________________________ 4. These types of casts are by far the most common _______________________________________ urinary casts. They are composed of solidified Tamm-Horsfall mucoprotein and secreted from _______________________________________ tubular cells under conditions of oliguria, _______________________________________ concentrated urine, and acidic urine. _______________________________________ _______________________________________ _______________________________________ 5. These types of casts are pathognomonic of acute tubular necrosis (ATN) and at times are 3. What are the major types of urinary casts? described as “muddy brown casts”. _______________________________________
    [Show full text]
  • Drug Induced Nephropathy Cases
    Drug Induced Nephropathy Cases 1. H.H., 43 y.o., 80 kg male being treated for gram-negative septic shock • Admitted to hospital 6 days ago, and has spent the last 3 days intubated in the ICU because of hypotension, respiratory failure, and altered mental status. On admission, H.H. was started on ceftriaxone 2 g IV daily, gentamicin 140 mg IV q8h. • Admission labs: – BUN 13 mg/dL (5-20) – SCr 0.9 mg/dL (0.5-1.2) – Serial, blood, urine, and sputum cultures were positive for Acinetobacter baumanii sensitive to ceftriaxone and gentamicin. • Current medications – Ceftriaxone 2 g IV daily – Gentamicin 140 mg IV q8h. – Norepinephrine IV 18 mcg/min – Pancuronium 0.02 mg/kg IV q3h – Famotidine 20 mg IV q12h – Lorazepam IV 2 mg/hr • Today (hospital day 7) vital signs: – Temp 101.5 F (38.6 C) – BP 90/40 mmHg – Pulse 135 beats/min – Respirations 20 breaths/min • Labs: • BUN 67 mg/dL • SCr 5.4 mg/dL • WBC 16,700 cells/mm3 • Urinalysis: – Many WBC (0-5) – 3% RBC casts (0-1%) – Granular casts – Osmolality 250 mOsm/kg (400-600) • Serum gentamicin with last dose: – Peak 15 mg/dL (target 6-10) – Trough 9.1 mg/dL (target <2) a) Circle the renal parameters that are abnormal. b) What drug is most likely associated with the abnormal renal labs? 1 c) What information did you use to arrive at your assessment? 2. J.S., 50 y.o. female with cellulitus • In hospital blood and wound cultures were positive for methicillin-sensitive Staphylococcus aureus • Received 2 full days nafcillin 2 g IV q4h and then was discharged home on dicloxacillin 500 mg PO QID x 14 d • 10 days post discharge, J.S.
    [Show full text]
  • Diagnosing Drug-Induced AIN in the Hospitalized Patient: a Challenge for the Clinician
    Clinical Nephrology, Vol. 81 – No. 6/2014 (381-388) Diagnosing drug-induced AIN in the hospitalized patient: A challenge for the clinician Mark A. Perazella Perspectives Section of Nephrology, Yale University School of Medicine, New Haven, CT, USA ©2014 Dustri-Verlag Dr. K. Feistle ISSN 0301-0430 DOI 10.5414/CN108301 e-pub: April 2, 2014 Key words Abstract. Drug-induced acute interstitial 5, 6]. As such, healthcare providers must be urine microscopy – eo- nephritis (AIN) is a relatively common cause knowledgeable in the diagnostic evaluation sinophiluria – leukocytes of hospital-acquired acute kidney injury of AKI to be able to differentiate these vari- – white blood cell cast (AKI). While prerenal AKI and acute tubular ous entities. This is particularly important as – acute kidney injury – necrosis (ATN) are the most common forms acute interstitial nephritis of AKI in the hospital, AIN is likely the next AKI is a growing problem in the hospital and – acute tubular necrosis most common. Clinicians must differentiate its incidence continues to increase [1]. Simi- the various causes of hospital-induced AKI; larly, the prevalence of AIN, primarily due to however, it is often difficult to distinguish drugs (> 85%), also appears to be increasing AIN from ATN in such patients. While stan- as a cause of hospital-acquired AKI [6]. dardized criteria are now used to classify AKI into stages of severity, they do not permit Since AKI is linked to untoward out- differentiation of the various types of AKI. comes such as incident and progressive This is not a minor point, as these different chronic kidney disease (CKD), end-stage AKI types often require different therapeutic renal disease (ESRD), and death, it is all the interventions.
    [Show full text]