Female with Protein Losing Nephropathy

Post Reply
Lynx

Post   » Thu Oct 22, 2015 8:58 pm


ph08fhf posted Barbara's necropsy on thread:
https://www.guinealynx.info/forums/viewtopic.php?t=72236

PRESENTING COMPLAINT:
Recheck protein losing nephropathy

HISTORY:
Barbara, a 4 1/2 year old female intact guinea pig, was initially presented to the Cornell University Hospital for Animals Exotics Service on 5/4/15 for a fluffed and hunched posture, which continued and was further evaluated on 8/27/15. At this recheck in August, Barbara was diagnosed with Protein Losing Nephropathy (Severe) and Ovarian Cysts (Left Ovary, Small) along with ventrally dependant pitting edema. At that time abdominal ultrasound and blood work confirmed these diagnoses. Barbara was prescribed Enalapril, Tramadol and Omega 3 supplements. Since the last visit, Barbara has had a good appetite, energy level and attitude. She has had occasional soft stools which cake onto her back end. She is weighed daily and her family has noted that as the ventral edema has decreased, so has her body weight. The family is still concerned about her hunched up, fluffed posture (seen in her up to 5 times per day) and are concerned that they have not seen her lay down, likely due to discomfort, in the last week. Barbara is currently housed with 9 other guinea pigs and is fed an assortment of timothy hay based pellets, blue grass hay, and vegetables.

VISIT SUMMARY:
On presentation, Barbara was bright, alert and responsive. Her heart rate was within normal limits and sounded strong and clear, with no murmurs or arrythmias noted. There was mildly increased respiratory sounds on auscultation and a slight abdominal component to her breathing. She was underconditioned, with a Body Condition Score of 2/9 (5/9 ideal), with abdominal distention (fluid filled) and ventral edema (fluid in her subcutaneous tissues) extending from her pubis to her neck.

After discussing Barbara's apparent continued good quality of life, and that the goal of treatment is to maintain this in the face of a poor long-term prognosis for severe protein losing nephropathy, it was decided to proceed with an ultrasound-guided cystoscentesis (using a needle to retrieve a sterile urine sample from her bladder) for culture (to rule out kidney infection) and urine protein creatinine ratio (UPC - to assess degree of protein loss), and recheck chemistry panel to assess kidney values while on enalapril.

Barbara's bladder was too small for safe cystocentesis therefore a catheter was passed into her urethra to obtain a sample of urine. This procedure was able to be done quickly and without complication. The first two attempts to retrieve peripheral blood (from lateral saphenous and cephalic) yeilded clotted samples that could not be read in house. A third attempt was made successfully, with Barbara in dorsal recumbency and accessing the cranial vena cava. On recovering Barbara from dorsal recumbency, she collapsed and became non responsive. Cardiopulmonary resuscitation was started immediately, including placement of a catheter into the trachea for ventilation and administration of epinephrine. No response to therapy was seen and resuscitation attempts were stopped after consultation with Ms. Fairbairn. A post mortem evaluation was requested to learn more about Barbara's cause of death and her protein losing nephropathy.

We are so sorry for your sudden loss. Barbara was a sweet girl and it was an honor to be part of her medical team. We know she will be greatly missed.

We also want to thank you for allowing us to perform a necropsy on Barbara. We hope that through Barbara we can learn more about this kidney disease in order to help other piggies in the future. We will be sure to keep you informed of our findings.

Please do not hesitate to contact us at any time with questions or concerns. Again, please know that we are thinking of you.

DIAGNOSTIC TESTING RESULTS:

Recheck Chemistry Panel:
Test Name: 8/27/15 Result>>>>>9/15/15 Result

Sodium (mEq/L) 145>>>139
Potassium (mEq/L) 7.3>>>8.9
Chloride (mEq/L) 108>>>94
Bicarbonate (mEq/L) 31>>>31
Anion Gap (mEq/L) 13>>>23
Na/K Ratio 20>>>16
Urea Nitrogen (mg/dL) 29>>>54
Creatinine (mg/dL) 1.1>>>2.1
Calcium (mg/dL) 12.0>>>12.5
Phosphate (mg/dL) 1.2>>>2.0
Total Protein (g/dL) 3.7>>>3.2
Albumin (g/dL) 1.6>>>1.4
Globulin (g/dL) 2.1>>>1.8
A/G Ratio 0.8>>>0.8
Glucose (mg/dL) 124>>>270
ALT (U/L) 27>>>27
AST (U/L) 71>>>100
Alkaline Phosphatase (U/L) 41>>>27
GGT (U/L) 3>>>5
Total Bilirubin (mg/dL) 0.0>>>0.0
Direct Bilirubin (mg/dL) 0.0>>>0.0
Indirect Bilirubin (mg/dL) 0.0>>>0.0
Amylase (U/L) 5101>>>5142
Cholesterol (mg/dL) 37>>>39
Creatine Kinase (U/L) 1135>>>2800
Iron (ug/dL) 174>>>144
TIBC (ug/dL) 187>>>176
FE saturation (%) 93>>>82
Lipemia 10>>>5
Hemolysis 59>>>18
Icterus 0>>>0

Total Protein-Creatinine Panel:
Protein Quantitative (mg/dL) 226.0
Creatinine (mg/dL) 7.5
T.Protein Creatinine Ratio 30.1

Urine Culture (Catheterized Sample):
No growth

Final Necropsy Report (at the request of Ms. Fairbairn):
Final Pathology Diagnosis:
Chronic progressive nephropathy

Histologic Morphologic Diagnosis:
Kidney: Severe, diffuse, chronic glomerulonephropathy with glomerular loss and synechia, periglomerular fibrosis, tubular degeneration and regeneration, marked tubular ectasia, tubuloproteinosis, tubular casts, hyaline droplets, and chronic interstitial nephritis

Lung: Mild, diffuse, chronic, eosinophilic and lymphoplasmacytic bronchiolitis and pneumonia with emphysematous change, osseous metaplasia and pulmonary edema.
Liver: Mild, multifocal, subacute, lymphocytic cholangitis

Heart:
1; Myxomatous degeneration of the left atrioventricular valve (low grade)
2; Mild, diffuse, chronic, epicarditis with fibrous connective tissue and rare Anitschkow cells.

Gastrointestinal tract: Mild to moderate, diffuse, chronic, histiocytic and lymphoplasmacytic enterocolitis and mucoid enteropathy

Gall bladder: Mild, diffuse, chronic, lymphocytic cholecystitis

Adrenal: Mild multifocal, subacute, adrenalitis with rare individual necrotic cells, lipofuscin and extramedullary hematopoiesis

Final Comment:
The histological findings are consistent with the chronic progressive nephropathy, similar to the well described entity in the aging rat.

Histologic Description:
LIVER (Slide 1; 3 sections): Multifocally in portal tracts, surrounding the bile ducts and rarely migrating into bile duct walls is a moderate infiltrate of lymphocytes admixed with rare heterophils. Partially occluding the lumen of blood vessels in portal tracts are occasional fibrin thrombi. Diffusely in the hepatocytes the cytoplasm contains cytoplasmic vacuoles which are the size of the nucleus or larger and the vacuoles displace the nucleus to the periphery of the cell (macrovesicular lipidosis).

LUNG (Slide 1; 2 sections): In the parenchyma are two small foci of osteoid production (osseous metaplasia). Multifocally, there is rare mild emphysema characterized by confluent alveolar spaces with shortened alveolar septa with blunt, clubbed ends. Multifocally, within alveolar spaces there is a mild infiltrate of heterophils. Within mildly thickened alveolar septa is a diffuse mild infiltrate of heterophils admixed with fewer plasma cells and lymphocytes. The adventitia of the blood vessels are diffusely widened up to three times the normal thickness, pale and loosely arranged (edema).

SPLEEN (Slide 1; 1 section): WNL

GALL BLADDER (Slide 2, 1 section): In the lamina propria is a mild diffuse infiltrate of lymphocytes.

SMALL INTESTINE (slide 2; 1 section): The submucosa is expanded by a mild diffuse infiltrate of macrophages admixed with fewer lymphocytes and heterophils. In the crypts are large number of goblet cells.

LARGE INTESTINE (Slide 2; 1 section): Same as small intestine

ADRENAL (Slide 2; 1 section): Within Normal Limits (WNL)

CEREBELLUM (Slide 3, 1 section): WNL

CEREBRUM (Slide 3, 1 section): WNL

KIDNEY (Slide 4; 3 sections): All levels of the nephron are diffusely affected. There is a mild reduction in the number of glomeruli. Multifocally, arterial walls are thickened and glomeruli have one or more of the following changes: variable thickening of Bowman’s capsule, periglomerular fibrosis, multifocal adhesions of the glomerular tuft to Bowman’s capsule (synechia), and dilated urineferous spaces. Occasionally, glomeruli contain variable amounts of eosinophilic proteinaceous material in urineferous space. Diffusely within the cortex and medulla, tubule epithelial cells have one or more of the following changes: marked thinning of the epithelial cells with dilated lumen, microvacuolated hypereosinophilic cytoplasm (degeneration), and frequent hyaline droplets; markedly ectatic with attenuation and loss of epithelium; or abundant basophilic cytoplasm with large nuclei, and occasionally pile up and form irregular tubules (regeneration) with thickened basement membranes. Multifocally, ectatic tubules contain variable amounts of pale to brightly eosinophilic proteinaceous casts, basophilic granular material (mineralized debris), sloughed epithelial cells, cellular and karyorrhectic debris, degenerate neutrophils, and rare erythrocytes. Multifocally, varibly sized cystic expansions of both tubules and glomeruli range less than 1 mm to 7 mm in diameter, lined by a single layer of cuboidal cells and are filled with homogeneous fluffy transparent fluid (mucus). Diffusely, the interstitium is moderately expanded by fibrosis, edema, and low numbers of lymphocytes and plasma cells. Multifocally, the capsular surface is irregular.

UTERUS (Slide 4; 3 sections): WNL

HEART (slide 5; 2 sections): On one section there is a locally extensive area of hemorrhage. On the other section is a focal area of loss of myocytes, replaced by fibrous connective tissue and fibroblasts admixed with few plasma cells and red blood cells. Rare Anitschow cells are noted around the area, interpreted as an attempt at myocardial regeneration. The left atrioventricular valve is widened by the accumulation of myxomatous ground substance and proliferation of sppindle cells arranged in a loosely organized nodules. The fibrous layer of the valve leaflets is not apparent, interpreted as collagen degeneration and loss. A focal area of osseous metaplasia in present in the fibrous ring at the base of the left atrioventricular valve.

Post Reply 1 post • Page 1 of 1