Case of the Month: January 2018: Kidney Injury in a Patient with Prior History of Drug Abuse and p-ANCA Associated Vasculitis

Case submitted by: David S. Priemer, MD1 (fellow), Jacquelynn T. Swan, MD2, and Carrie L. Phillips, MD1

Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana1, and Hendricks Regional Hospital, Avon, Indiana2, USA

Clinical History

A 38-year-old woman presented to the Emergency Department following a generalized seizure that was preceded by at least several days of increasing confusion. She was a poor historian; however, her past medical history was significant for chronic substance abuse and perinuclear anti-neutrophil cytoplasmic antibody (p-ANCA) associated vasculitis treated with systemic steroids four years prior to her most recent presentation. Tissue biopsy had not been previously performed. Initial laboratory tests were most remarkable for an elevated serum creatinine of 11.31 mg/dL, leukopenia (white blood cell count of 2.9 k/mm3), and neutropenia (1.3 k/mm3). Serologic studies were positive for p-ANCA but negative for cytoplasmic (c)-ANCA. Autoantibodies were elevated for myeloperoxidase (MPO) and anti-proteinase 3 (PR3). Anti-nuclear antibody (ANA) was measured at the upper limit of normal. Serum complement C3 and C4 levels were low at 59 mg/dL and 12 mg/dL, respectively. Titers for PLA2R and THSD7A were not determined. Remaining laboratory studies are tabulated below. The patient was admitted for renal replacement therapy. After five days of hemodialysis a renal biopsy was performed.

 

Table 1. Patient Laboratory Studies

Laboratory study Result
White blood cell count 5.4 k/mm3
Hemoglobin 8.8 GM/dL (L)
Hematocrit 26.4%
Platelets 177 k/mm3
Sodium 138 mmol/L
Potassium 4.7 mmol/L
Chloride 107 mmol/L
Calcium 8.4 mg/dL (L)
Phosphorus 6.6 mg/dL (H)
Blood Urea Nitrogen 70 mg/dL (H)
Creatinine 11.31 mg/dL (H)
Estimated glomerular filtration rate 4 mL/min/1.73m2 (H)
Glucose H 107 mg/dL (H)
Urine specific gravity 1.010
Urine pH 7.0
Urine Protein >500 mg/dL (H)
Urine Glucose 150 mg/dL (H)
Urine Ketones Negative
Urine Red Blood Cells 50-100/high-power field (H)
Urine Hemoglobin 70 Ery/µL (H)
Urine urobilinogen and bilirubin Negative
Urine White Blood Cell Esterase, bacteria, and nitrites Negative
C3 Complement 59 mg/dL (L)
C4 Complement L 12 mg/dL (L)
ANA Titer 1:40
Myeloperoxidase antibody >8.0 Units (H)
Proteinase 3 antibody 0.6 Units (H)
perinuclear-ANCA Positive
cytoplasmic-ANCA Negative

Abnormal values are indicated by H = high; L = low.

 

Renal biopsy findings:

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Figure A. Jones’ silver stain shows widespread spikes and vacuoles along basement membranes of glomerular capillary loops. Periglomerular fibrosis is present. Vascular pole is near bottom left and urinary pole is near top right. Original magnification is 600x.
Figure B: Periodic acid-Schiff stain highlights segmental obliteration of capillary loop basement membranes (right side of glomerulus shown). Original magnification is 600x.
Figure C: Lillie’s allochrome stain highlights obsolescent glomeruli (arrows point to three) surrounded by tubular atrophy and interstitial fibrosis. Some tubule lumina contain cell debris or proteinaceous casts. The unlabeled glomerulus at left of center shows segmental sclerosis. Original magnification is 200x.
Figure D. Immunofluorescent and electron microscopy.
Ultrastructural examination shows thickening and distortion of glomerular basement membranes by numerous subepithelial electron-dense deposits (black arrow) defined by spikes and caps of extracellular matrix. The podocyte at top shows effacement of foot processes, which was widespread in the glomeruli examined. Immunofluorescence of OCT-embedded frozen tissue sections shows intense, diffuse granular labeling of glomerular capillary loops with antibodies to immunoglobulin G (IgG, inset, white arrow), complement C3, and equal kappa and lambda light chains. Antibodies directed to IgA, IgM, complement C1q, albumin, and fibrinogen lacked specific reaction (not shown).

At least 45 glomeruli were sampled in sections from formalin-fixed, paraffin-embedded renal tissue, of which 33 were obsolescent (73.3%). The remaining glomeruli showed variable mesangial matrix expansion but lacked nodularity. Glomerular capillary loops were remarkable for spikes and vacuoles (figure A) along basement membranes including some with segmental collapse and capsular adhesions (figure B). Crescents were not seen. Other findings included a significant degree of tubular atrophy and interstitial fibrosis (figure C) with monocellular interstitial inflammatory infiltrates.

Interpretation: The findings were consistent with membranous glomerulopathy, with secondary focal segmental glomerular sclerosis.  Features diagnostic of active vasculitis were not seen.

Question:

The patient’s urine drug screen and blood toxicology were positive. Adulteration of which of the following drugs of abuse has been associated with this patient’s renal disease?

  1. Heroin
  2. gamma-Hydroxybutyric acid
  3. Methamphetamine
  4. Cocaine
  5. 3,4-Methylenedioxymethamphetamine (MDMA)

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Clinical Presentation:

The patient is a 73 year-old female who presented with acute kidney injury while on chemotherapy for metastatic urothelial carcinoma.  She initially presented with a symptomatic deep vein thrombosis.  At this time laboratory testing revealed elevated serum creatinine that increased from 3.1 mg/dL at presentation to 4.0 mg/dL over two days from a known baseline of 0.8 – 1.0 mg/dL, prompting a renal biopsy.

Urinalysis showed moderate blood and the urine protein/creatinine ratio was 1.5mg, along with white blood cell casts, but no red blood cells. Hemoglobin was 9.1 g/dL and serum albumin measured at 3.0 g/dL. There was no evidence of eosinophilia, rash or fever.

One year prior, following her initial diagnosis of metastatic carcinoma, the patient underwent six cycles of Gemcitabine and Carboplatin, which was completed six months prior to presentation. She was subsequently started on Pembrolizumab, a PD-1 (programmed cell death 1) inhibitor, two weeks prior to presentation. The patient also has a history of rheumatoid arthritis treated intermittently with Ibuprofen.

Renal Biopsy Images:

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Figure 1: Diffuse interstitial inflammation accompanied by mild edema and frequent tubulitis. [H&E] x 200
Figure 2: On higher power, the interstitial infiltrate is composed of activated lymphocytes, neutrophils, macrophages and frequent eosinophils. [H&E] x 400
Figure 3: Immunoperoxidase staining reveals over 95% of the infiltrating interstitial mononuclear cells are CD 3 positive T lymphocytes. [CD 3 IHC] x 400
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Figure 4: Immunoperoxidase staining reveals with only few scattered CD 20 positive B lymphocytes. [CD 20 IHC] x 400
Figure 5: On electron microscopy, tubular lining cells display varying degrees of epithelial injury with infiltrating mononuclear inflammatory cells. [EM] x 3500
What is your  Diagnosis?

  1. Acute pyelonephritis
  2. Drug-induced hypersensitivity tubulointerstitial nephritis
  3. Sjögren syndrome
  4. IgG4 related tubulointerstitial nephritis
  5. Anti-tubular basement membrane antibody nephritis

Case submitted by:

Ryane N. Panasiti, MD, Clinical Fellow, Department of Nephropathology, University of North Carolina, Chapel Hill, NC, USA

Sharon Latcha, MD, Division of Nephrology, Memorial Sloan Kettering Cancer Center, NY, USA

Surya V. Seshan, MD, Department of Pathology, Weill Cornell Medicine, NY, USA

 

What is your diagnosis? Chronic kidney disease and accelerated rise in creatinine

The patient is a 55-year-old man with a history of type 2 diabetes, autoimmune pancreatitis, GERD and hypertension. He has known chronic kidney disease stage III; however, recently creatinine rapidly rose (2.1-3.2-3.9) in four months. C3 is low (89) but C4 is normal. Additional tests demonstrated very elevated IgG, IgE and increased IgG4 subclass. ESR was 111mm/hour.

Figure 1, H&E, 40x magnification shows a low power view of renal cortex with a dense interstitial fibrosclerosis obliterating tubules, surrounding intact glomeruli, with a sharp, abrupt transition to normal tubules.

 

Figure 2, H&E, 200x magnification shows a lymphoplasmacytic infiltrate embedded within a background of patchy storiform fibrosis. Remnant tubules are barely perceptible.

 

 

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Figure 3, H&E, 200x magnification shows less fibrotic areas with denser lymphoplasmactyic infiltrate, numerous eosinophils, and atrophic tubules.

 

Figure 4, IHC IgG 400x magnification highlights numerous plasma cells within the inflammatory infiltrate

 

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Figure 5, IHC IgG4, 400x magnification shows that nearly all the IgG positive plasma cells are IgG4 subtype

 

WHAT’S YOUR DIAGNOSIS?

1) Drug-induced acute interstitial nephritis
2) Chronic pyelonephritis
3) Lupus tubulointerstitial Nephritis
4) IgG4-related tubulointerstitial Nephritis
5) Lymphoma

Contributed by:

Serena Tan, MD and Megan Troxell, MD PhD

Department of Pathology, Stanford University School of Medicine, Stanford CA

What is your Diagnosis? A 76 year-old woman with acute renal failure.

A 76-year-old woman presents with acute renal failure. She reports a 30 lb unintentional weight loss over the past few months. Her laboratory data show serum creatinine of 2.5 mg/dL and mild proteinuria (1 g/g) with microscopic hematuria. The images from her renal biopsy specimen reveal refractile intratubular casts. On immunofluorescence, the casts stain strongly for kappa light chain and are negative or weakly positive for lambda light chain.

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Figure 1. Low-power. Acute tubular injury.
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Figure 2. Hi-power. Tubular casts.
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Figure 3. IF: kappa
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Figure 4. IF: lambda

The most likely cause for the patient’s acute renal failure is:

A. Acute pyelonephritis
B. Chronic kidney disease with hyaline casts
C. Myeloma cast nephropathy
D. Ischemic acute tubular necrosis
E. Rhabdomyolysis

Case presented by David Cimbaluk, MD
Assistant Professor of Pathology
Rush University Medical Center, Chicago, IL

July 2017: A cracking case

Case submitted by: Maria F S Soares, Michael Reschen, Ian S D Roberts
Oxford University Hospitals NHS Foundation Trust – Oxford – UK

Clinical history

A 59 year-old woman presented with nephrotic syndrome for 6 weeks. She had no significant past medical history. She had pitting leg oedema and blood pressure 130/90 mmHg. Bilateral pleural effusion were seen by chest X-ray and CT. Serum albumin was 33 g/L (normal >36g/L), serum total cholesterol was 11 mmol/L (424.7 md/dL) and the urine protein-to-creatinine ratio (uPCR) was 485.8 mg/mmol (3.23 g/day). Urine dipstick showed haematuria and proteinuria. Serum creatinine was 76 micromol/l (0.86 mg/dL). She was referred to the nephrology clinic with persistent nephrotic syndrome and hypertension, despite treatment with furosemide and ramipril. Serologic workup was negative. A left sided percutaneous renal biopsy was performed.

Renal Biopsy Findings

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Figure 1. Tip lesions were found. No proliferative lesions were seen.

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Figure 2. Albeit congested, glomerular capillaries showed normal appearance on H&E and silver stain (not shown).

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Figure 3. Minimal chronic damage was seen.

Figure 4. There was tubular vacuolation in keeping with proteinuria.

Figure 5. Scanty red cell casts were seen. Immunofluorescence staining was negative for IgG, IgA, IgM, C3, C1q and light chains. Electron microscopy showed diffuse foot process effacement. No electron dense deposits were observed. Glomerular basement membranes were of normal thickness; no splitting was found.

Based on these findings, what is the most likely cause of the patient’s hematuria?

1- FSGS, tip lesion variant
2- Pre-spike stage membranous glomerulonephritis
3- Collagen type IV nephropathy
4- Renal vein thrombosis
5- Other

Case of the Month: June 2017: Acute kidney injury in an renal transplant patient

Liying Fu, MD., Ph.D.

Ruffolo, Hooper & Associates, M.D., P.A,  and Tampa General Hospital, Tampa, FL, 33634

A 45-year old Caucasian woman with past medical history of type 1 diabetes mellitus and end-stage renal disease underwent kidney and pancreas transplant with insertion of ureteral stent five months ago.  The kidney transplant was from a male donor in his 30’s who died of anoxia.  This was a CMV + to + and EBV + to + match.

She was admitted with acute kidney injury, with serum creatinine rising from 1.2 to 2.5 mg/dL, accompanied by hematuria.  Urinalysis on admission was positive for large hemoglobin, red blood cells and protein.  Urine protein:creatinine ratio was 3.12. DSA was negative and renal ultrasound revealed patent renal transplant vasculature.  CMV and plasma BK virus PCR were negative but urine adenovirus PCR was positive.  A kidney transplant biopsy showed the following findings:

 

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Figure 1. Renal cortex shows a patchy mild lymphocytic interstitial infiltrate with focal mild tubulitis. No neutrophils or granulomatous inflammation are seen. The tubules show focal acute tubular injury and a few Tamm-Horsfall protein casts (H&E, 100x).
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Figure 2. Toluidine-stained sections of tissue submitted for electron microscopy show a dense interstitial infiltrate with mononuclear cells and granulomas surrounding the necrotic tubules (200x).
Figure 3. Some of the tubular epithelial cells and interstitial cells show nuclear enlargement with possible cytoplasmic and nuclear viral inclusions in toluidine-stained sections of tissue submitted for electron microscopy (400x).
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Figure 4. Transmission electron microscopy reveals closely packed viral particles in the cytoplasm of tubular epithelial cell (27,000x).
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Figure 5. Transmission electron microscopy reveals hexagonal virus particles of 70–80 nm in diameter, closely packed in a crystalline array, in the cytoplasm of tubular epithelial cells and cells in interstitium (54,000x).

 

WHAT IS YOUR DIAGNOSIS?

  1. Acute cellular rejection
  2. BK virus nephropathy
  3. Cytomegalovirus nephropathy
  4. Adenovirus nephritis
  5. Other acute interstitial nephritis

Case of the Month: May 2017: A rare cause of proteinuria.

Case submitted by: Naima Al Alawi, MD, Nephropathology Fellow, Rajib K Gupta, Nephropathology Fellow, Naima Carter-Monroe, MD, MHS, Instructor in Pathology, and Lois Arend, PhD, MD, Associate Professor.

Division of Kidney-Urologic Pathology, Department of Pathology, Johns Hopkins Hospital and Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

 

Clinical Presentation: An African American female in her thirties presented with 3 grams of proteinuria and normal serum creatinine. She had a known medical history significant for dysautonomia-induced gastroparesis and bilateral hydronephrosis.  Moreover, she had presented 6 months prior with 2.5 grams of proteinuria, low C3 and a creatinine of 0.8 mg/dl. All serologies were negative except for a positive anti-Ro at that time. A renal biopsy at this earlier presentation (not shown) demonstrated granular mesangial and rare capillary wall staining for IgG, IgM, IgA, C3, and C1q (“full-house”), by immunofluorescence microscopy, with small mesangial electron-dense deposits and rare subepithelial and intramembranous densities by electron microscopy, consistent with class II lupus nephritis. However, the possibility of renal involvement by other autoimmune disease process, such as mixed connective tissue disorder, could not be excluded. A repeat kidney biopsy was performed at this admission.

Fig 1: H&E stain, 400x magnification, showing a single glomerulus with mild mesangial expansion and minimal thickening of capillary walls.
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Fig 2: Silver stain, 400x magnification, showing a single glomerulus with segmental silver-negative holes or bubbles within its capillary walls.
Fig 3: Immunofluorescence for IgG, 400x magnification, showing linear non-specific 2-3+ staining.
Fig 4: Electron microscopy, 8000x magnification, showing a capillary loop with marked podocyte injury, characterized by foot process effacement and microvillous transformation of podocyte cytoplasm.
Fig 5: Electron microscopy, 30,000x magnification, showing a capillary basement membrane with numerous microspherical and microtubular structures (average diameter of 49 nm by morphometric measurement), with overlying flattened foot process also showing focal microfilament hypertrophy.

What is the most likely diagnosis based on this biopsy?

  1. Lupus nephritis class II
  2. Resolving membranous glomerulopathy
  3. Proliferative lupus (class III or IV) nephritis
  4. Lupus nephritis class V
  5. Podocyte infolding glomerulopathy

Case of the Month: April 2017: Sudden onset of edema and renal insufficiency in a 50-year-old-man

Case submitted by:

David Cimbaluk, MD. Assistant Professor of Pathology, Rush University Medical Center, Chicago, IL

Clinical Presentation: 

A 50-year-old man presented with generalized edema.  Past medical history was significant for colon cancer 1 year ago treated by surgical resection alone (no chemotherapy).  On physical exam, blood pressure was 112/70 mmHg.  Auscultation of the lungs revealed bilateral rales.  He had abdominal ascites and 3+ leg edema.  Laboratory workup showed serum creatinine 1.9 mg/dl, urinalysis showed 3+ protein, 1+ blood, and protein/creatinine ratio of 0.5 g/g.  Secondary serological workup was negative. A renal biopsy was performed.

Figure 1 – Hematoxylin and eosin (H&E) stain, 200x magnification, shows a glomerulus with a bloodless, consolidated appearance, a mild increase in cellularity, and no thrombi.
Figure 2 – Hematoxylin and eosin (H&E) stain, 400x magnification, shows a glomerulus with glomerular capillaries occluded by swollen endothelium and thickening of the glomerular capillary walls.
Figure 3 – Periodic acid-Schiff stain, 400x magnification, shows a glomerulus with capillary lumens obliterated by endothelial swelling, increased cellularity in areas, and the glomerular basement membranes are duplicated in focal areas.
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Figure 4 – Jones methenamine silver stain, 400x magnification, shows segmental glomerular basement membrane remodeling with replication of capillary wall basement membranes.
Figure 5 – Negative immunofluorescence for all reagents tested (IgG, IgA, IgM, K/L light chains, C3, C4,
C1q, albumin, fibrinogen).
Figure 6 – Ultrastructural examination, 30,000x magnification, showing the glomerular capillary lumen occluded by endothelial swelling, electron-lucent widening and subendothelial flocculent material. The endothelial cell fenestrations are lost. Podocyte foot processes are preserved.
Figure 7 – Ultrastructural examination, 30,000x magnification, showing the glomerular capillary lumen is completely occluded by endothelial swelling. The subendothelial zone is expanded and contains flocculent material. Podocyte foot processes are focally effaced.

What’s your Diagnosis?

A. Membranoproliferative glomerulonephritis

B. Postinfectious glomerulonephritis

C. Glomerular endotheliosis

B. Lupus nephritis

 

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Case submitted by:

Susanna A McRae, MD, FRCPC, renal pathology fellow and David George, MD, FRCPC, Department of Pathology, Foothills Medical Centre and University of Calgary School of Medicine, Calgary, Alberta, Canada.

Clinical presentation

The patient is a 24-year-old male competitive body builder who presented with a two week history of peripheral edema and 20 lb weight gain. He admitted to taking various supplements, including “mild anabolic steroids” and diuretics before competitions to increase muscle definition.  He purposefully pursued a high-protein diet.  He had a history of non-obstructive renal calculi, without hydronephrosis.

The patient was noted to be very muscular, with a BMI of 29.  Blood pressure was 130/90, and there was mild peripheral edema in his lower limbs.  Urinalysis showed > 3 g/L protein and moderate blood by dipstick.  Laboratory studies revealed creatinine 145 umol/L (1.6 mg/dL, GFR 58), urine protein-creatinine ratio of 947 mg/mmol, and serum albumin 10 g/L.   A year previously, the creatinine had been 91 umol/L (1.0 mg/dL, GFR 101).   A renal biopsy was scheduled for a month later, but in the interim the patient chose to self-medicate with diuretics to prepare for a body-builder exhibition.   Diuretic use was associated with a transient rise in the serum creatinine to 215 umol/L (2.4 mg/dL), followed by a decline to 172 (1.9 mg/dL) at the time of biopsy.  Hepatitis BSAg and antibodies to Hepatitis C were negative; HIV status was not determined.  Anti-nuclear antibody was negative and C3 and C4 were in the normal range.

 

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Figure 1: Masson Trichrome stain, 40x magnification, demonstrating approximately 40% interstitial fibrosis and tubular atrophy.
Figure 2: Masson Trichrome stain, 100x magnification, showing one of the few glomeruli without sclerosis, adjacent to 2 glomeruli with segmental sclerosis, definitely perihilar in one. The non-sclerotic glomerulus is hypertrophic: diameter 240 um.
Figure 3: Periodic acid-Schiff (PAS) stain, x200 magnification, demonstrating two glomeruli with segmental sclerotic lesions adjacent to the hilum, with extension into the hilar arterioles. The biopsy contained 12 glomeruli, 4 globally or subtotally sclerosed, and 6 with segmental sclerosis that was perihilar in 5 and indeterminate in one. No collapsing FSGS was identified. Only two glomeruli lacked sclerosis.
Figure 4: Jones’ silver stain, x200 magnification, demonstrating two glomeruli with segmental sclerotic lesions adjacent to the hilum, with extension into the hilar arterioles.
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Figure 5: Immunofluorescence microscopy for IgM, 400x magnification, showing 2+ (scale 0-4+) smudgy perihilar segmental staining. C3 staining was 3+, and C1q was 1+, both in a similar segmental pattern. IgG and IgA were negative.
Figure 6: Electron microscopy, 1000x magnification, showing about 70% foot process effacement. There was segmental sclerosis elsewhere, but no dense deposits.

What is your diagnosis?

  1. IgM nephropathy.
  2. Primary FSGS (NOS).
  3. FSGS, perihilar variant, secondary to anabolic steroid use.
  4. Hypertensive nephropathy.
  5. Alport Syndrome.

 


 

 

 

 

 

Case of the Month: February 2017: Acute kidney injury in a 68 year-old woman

CASE AUTHORS:

Paul Ndekwe, MD, Pathology Resident, Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN

Charles Carter, Jr., MD, Indiana Kidney Specialists, Indianapolis, IN

Arjun D. Sinha, MD, MS, Assistant Professor of Clinical Medicine, Department of Medicine, Division of Nephrology, Indiana University School of Medicine and Richard L. Roudebush VA Medical Center, Indianapolis, IN

Carrie L. Phillips, MD, Professor, Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN

CLINICAL HISTORY:

A woman in her seventh decade of life presented to our emergency department with confusion, slurring of speech, and gait imbalance.  She had a complicated medical history of chronic kidney disease, diabetes mellitus type II, essential hypertension (for 30 years), obesity, obstructive sleep apnea on CPAP, hypercholesterolemia, chronic anemia, gastroesophageal reflux, and polypharmacy.  During the previous five months she had multiple visits to clinics and emergency departments with similar symptoms plus progressive weakness and dyspnea on exertion. During these visits she had been diagnosed with bronchitis, mild aortic stenosis with stage II diastolic dysfunction, acute kidney injury (attributed to intravascular volume depletion and hypertension), Klebsiella urinary tract infection, and sepsis.  Nearly a decade before, she experienced a cerebrovascular accident with right-sided symptoms that eventually resolved.  Her past surgical history included a Roux-en-Y gastric bypass two years prior that was complicated by incisional hernias and a perforated ulcer.  She had undergone bilateral knee replacements three years prior and open reduction internal fixation of an arm fracture a decade ago.

Laboratory values included a positive urine WBC esterase (25  Leu/μL, normal range: negative), elevated urine white blood cell count (5-10/hpf, normal range: 0-5/hpf), trace urine bacteria, elevated urine protein (30mg/dL, normal range: negative), and an elevated serum creatinine  up to 4.04 mg/dL compared to baseline 1.07 mg/dL nine months prior, 1.50 mg/dL three months prior, and 3.02 mg/dL two week earlier (normal range: 0.6 – 1.2mg/dL).  A renal ultrasound was normal. The patient’s confusion and slurring resolved spontaneously during her hospital stay.  With discontinuation of losartan and intravascular volume expansion her serum creatinine improved.  She was discharged with a creatinine of 3.3 mg/dL.  She returned to the emergency department a week later with similar symptoms and a serum creatinine of 4.1 mg/dL.  Volume expansion again improved her renal function and she was discharged home with nephrology follow-up scheduled soon thereafter.  She was seen in follow-up, a serologic evaluation was performed, and she was scheduled for a renal biopsy in order to assess the underlying potential causes of her worsening renal function.

LIGHT MICROSCOPY IMAGES FROM THE RENAL BIOPSY SPECIMEN:

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Figure 1. H&E stained paraffin tissue section (400X magnification) shows interstitial non-necrotizing granulomatous inflammation with an adjacent Schaumann body (arrow).
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Figure 2. H&E stained section (400X magnification) shows poorly formed granuloma with giant cell (arrow).
Figure 3. H&E stained section (400X magnification) shows a giant cell containing a Schaumann body (arrow).

WHAT IS YOUR BEST DIAGNOSIS?

  1. Foreign body giant cell reaction due to intravenous drug use
  2. Acute and chronic pyelonephritis due to urinary tract infection
  3. Granulomatous interstitial nephritis
  4. Plasma cell dyscrasia
  5. Lupus nephritis