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Articles 2020-24 > Nephro > Flashcards

Nephro Flashcards

1
Q

What are the renal consequences of NSAID ?

A

NSAID rarely cause ARF, but common cause AKI.

Prostaglandins (PGE2, PGI2) are vasodilators of the afferent arterioles → increase renal perfusion → protect the medulla (vasa recta capillaries) against hypoperfusion and hypoxia.

NSAIDs → ⊖ prosta via COX-2.
- interstitial nephritis
- renal crest necrosis
- tubular necrosis

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2
Q

What are the extrinsic regulator of renal circulation ?

A
  • Autonomic NS : stimulated by exercise, excitement, shock → decrease renal blood flow → decrease GFR
  • Catecholamines : release of epinephrine, norepineprhine from the adrenal medulla → decrease renal blood flow → decrease GFR
  • Humoral factors :
    • Angiotensin II : potent vasocontrictor of efferent > afferent arterioles → stabilization of glomerular filtration p°
    • Endothelin : released from damaged endothelial cells → decrease renal cortical blood flow
    • PGE2, PGI2, NO : vasodilators
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3
Q

How the kidney can regulate systemic circulation ?

A

Via its production of renin and initiation of RAAS, and ADH-stimulated resorption of water in the collecting ducts → regulation of blood p°, volume and tonicity

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4
Q

What are the intrinsic regulator of renal circulation ?

A
  • Myogenic response : in the muscular wall of the afferent and efferent arterioles
  • Tubuloglomerular (TG) feedback mechanism : involve the juxtaglomerular apparatus (JGA), composed of granular cells (in the wall of afferent arterioles), extraglomerular mesangial cells, and macula densa cells (in the wall of DCT)
    • ↘︎ GFR → ↘︎ [NaCl] in the DCT → release of NO, prostagladins → vasodilation of afferent arteriole and secretion of renin from the granular C → stimulation of RAAS and constriction of efferent arteriole
    • ↗︎ GFR → ↗︎ [NaCl] in the DCT → release of ATP → vasocontriction of afferent arteriole

Autoregulation of renal blood flow to limit GFR variations until 25% variation in blood flow.

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5
Q

What is the effect of aldosterone ?

A

Aldosterone increase Na+ resorption from the distal tubules and collecting ducts → increase intravascular volume

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6
Q

What are the criteria of AKI ?

A

AKI = early and often non clinical renal injury. One or more criteria :
1- ↗︎ creat ≧ 0.3 mg/dL within 48h
2- ↗︎ creat ≧ 1.5x baseline within 7 days
3- oliguria of 6 hours duration despite adequate hydration status

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7
Q

What is ARF ?

A

Loss of ≧75% nephron function → decrease the ability to excrete waste products and maintain fluid and electrolytes homeostatis

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8
Q

Which part of the kidney is most susceptible to ischemic damage?

A

Tubular epithelial cells (TEC) of proximal tubules and the ascending loop of Henle : high metabolic rate and O2 demand for reabsorption and active transport → predisposed to ischemic injury in a context of low perfusion.

TEC receive O2 and nutrients from adjacent peritubular capillaries (vasa recta) localised after efferent arterioles

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9
Q

What are the consequences of ischemia on tubular cells ?

A

Loss of proximal tubule brush border → leakage into the interstitium → interstitial edema

Tubular cast formation → obstruction → increased intraluminal p°

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10
Q

Which ATB are nephrotoxic if administered to dehydrated or hypotensive horses ? Why ?

A

Aminoglycoside and tetracycline

During decreased urine flow → high concentration of nephrotoxic drug in the glomerular filtrate → increased absorption of the drug into the tubular epithelial cell → toxic effect of the drug.

Aminoglycosides → loss of prot. synthesis, decreased mitochondrial f° and cell death
Residual drug in circulation → toxicity during 2-3 days after adm°

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11
Q

What is vasomotor nephropathy ?

A

Vasomotor or sepsis-associated or hemodynamically-mediated nephropathy

Sepsis is responsible of microcirculation dysf° + inflamm° + coagulopathy → renal cortical necrosis with hemorrhage

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12
Q

What is pigment nephropathy ?

A

Due to hemoglobinuria or myoglobinuria
- Direct toxic effects on TEC with tubular casts
- Indirect (hemodynamic) effects → stimulation of sympathetic NS → catecholamines → decrease renal blood flow

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13
Q

What are the 3 common causes of AKI in horses ?

A
  • Ischemic
  • Nephrotoxic
  • Sepsis-associated or vasomotor
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14
Q

What are the 5 common causes of ARF in horses ?

A
  • Hemodynamic or vasomotor or sepsis-associated
  • Nephrotoxic → aminoglycosides, tetracyclines, biphosphonate, NSAID
  • Hemolysis, myopathy → hemodynamic + pigment nephropathy
  • Immune-related drug reaction (idiosyndratic)
  • Infectious → Leptospira spp.
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15
Q

Why BUN is not commonly used to assess renal function in horses ?

A

Urea is freely filtered and reabsorbed in the renal tubules, and influenced by numerous factors, including dietary protein and protein metabolism.
Creat, SDMA → freely filtered → estimating GFR
BUN/creat → not a reliable test for separating pre-renal from renal azotemia

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16
Q

What is the clinical significance of USG = 1.010 ?

A

When ≧ 2/3 loss of tubular f° → isosthenuric urine (1.008 -1.016)
If pre-renal azotemia → USG hypersthenuric

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17
Q

What are the urine cytologic findings with AKI ?

A
  • RBC
  • Tubular casts
  • WBC if infectious or inflammatory
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18
Q

What is the most common infectious cause of ARF ?

A

Leptospira spp
TT : β-lactam or enrofloxacin

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19
Q

What are the most common electrolytes abnormalities in horses with ARF ?

A

Hyponatremia, hypochloremia
+/- hyperkalemia, hypercalcemia, hypermagnesemia
+/- metabolic acidosis

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20
Q

What is the TT of ARF ?

A

1- TT of predisposing disease or stop nephrotoxic drugs
2- IV volume expansion with crystalloids
3- If oliguria/anuria → restore CVP → restore SBP → use furosemide

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21
Q

What is CKD ?

A

CKD = chronic, irreversible progressive disease (functional or structural), in progress for more than 3 months
≠ CRF which reflects an end-stage disease

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22
Q

What are the 3 categories of CKD ?

A
  • Tubulointerstitial disease = chronic interstitial nephritis : lesions of tubules → toxic, ischemic, SIRS, sepsis
  • Glomerulonephritis : deposition of Ab-Ag complexes to the glomerular basement membrane → infection with Leptospira, Strepto, EIA virus, purpura hemorrhagica or secondary to AKI and tubulointerstitial disease
  • End-stage renal disease
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23
Q

What are the most common clinical signs associated with CKD ?

A

Weight loss, PUPD, ventral edema
+/- hematuria, hypertension, uremic encephalopathy …

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24
Q

What is the clinical significance of urine protein-to-creatinin ratio (UPC) ?

A

Normal UPC < 0.5

If UPC > 2 → marked proteinuria → glomerulonephritis

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25
Q

What are the most common electrolytes abnormalities in horses with CKD ?

A
  • Hypo-Na, hypo-Cl
  • Hyper-K, hyper-Ca
  • Variable P (predominantly hypo-P)
  • Mild metabolic acidosis (pH < 7.35) : due to decreased H+ excretion and HCO3- prod° by kidney
  • Hypo-albuminemia, anemia
  • ↗︎ triglycerides
  • Hypertension : due to RAAS activation
    Normal NIBP : 135, 110, 90
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26
Q

What is the clinical utility of NGAL ?

A

Neutrophil Gelatinase-associated Lipocalin (NGAL) → filtered and completely reabsorbed in proximal tubules
Biomarker of tubular injury

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27
Q

DDX of red discolored urine ?

A
  • Hematuria
  • Hemoglobinuria
  • Myoglobinuria
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28
Q

What is the clinical significance of urine discoloration during the end of micturition ?

A
  • End of urination : proximal urethra or bladder neck
  • Beginning of micturition : distal urethra
  • Persistently discolored streams from beginning to end : renal, ureteral, bladder
29
Q

DDX of hematuria (14)

A
  • Exercise-induced hematuria : after strenous exercise, unrelated to bladder calculi → asympto, microscopic hematuria. Bladder trauma or increased glomerular permeability ?
  • Urolithiasis : cystic calculi → most common cause of post-exercise hematuria. Pollakiuria, stranguria, incontinence. ♂︎ > ♀︎
  • UTI : positive if > 10.000 cfu/mL. Most commonly Gram ⊖ → Proteus mirabilis, E. coli, Klebsiella spp., Enterobacter spp.
  • Idiopathic renal hematuria : acute onset of hemorrhage from 1 or both kidneys → nephrectomy. Arabians ++
  • Neoplasia : rare cause of hematuria. Kidney → nephroblastoma (young), adenocarcinoma (older) ; bladder → SCC
  • Verminous nephritis : Halicephalobus gingivalis → formation of renal granulomas. Nematode → invasion of kidneys, CNS, long bones, and eyes.
  • Idiopathic hemorrhagic cystitis : proliferative and hemorrhagic bladder mucosa (apex ++). Histo → neutrophilic and hemorrhagic cystitis. Favorable prognosis.
  • NSAID-induced ulcerative cystitis
  • NSAID-induced renal crest necrosis
  • Polypoid cystitis
  • Urethral rents : hematuria usually detected at the end of urination due to urethral contraction. Stallions and geldings.
  • Urethritis : usually secondary to trauma, bacteria, neoplasia, parasitic (Habronema)
  • Hematuria in foals : uncommon → trauma, urachus hematoma, UT obstruction or rupture, acute tubular necrosis, leptospirosis…
  • Cantharidin toxicity : blister beetle in alfalfa hay. Hematuria + oral erosion + GI pain + hypoCa
30
Q

DDX of hemoglobinuria

A

Due to intravascular hemolysis :
- Parasitic : piroplasmosis
- Viral : EIA
- Immune-mediated
- Toxic :
* Red mapple leaves, sudan grass
* Phenothiazine
* Copper
* Wild onion

31
Q

DDX of myoglobinuria

A
  • Trauma
  • Exertional myopathies
  • Immune-mediated myopathies (Strepto equi)
  • Post-anesthetic myoneuropathies
  • Atypical myopathy
  • Clostridial myonecrosis
  • Nutritional myodegeneration : due to selenium deficiency in foals
  • Toxins : ionophores
32
Q

Which disinfectant solution is the best to apply to the stump in foals ?

A

Dilute chlorexidine solution (0.5%) is more effective than 1% or 2% iodine solutions and is less irritant to the tissues.

33
Q

Which antibiotics should I choose for patent urachus associated with septic omphalitis/omphalophlebitis ?

A

Drugs that are eliminated in the urine : potentiated sulfonamides, aminoglycosides, penicillins
Second line : cephalosporins

34
Q

What are the congenital causes of urinary incontinence in foals ?

A
  • Congenital patent urachus
  • Septic omphalitis / omphalophlebitis
  • Ectopic ureter
35
Q

What is the treatment of UMN bladder dysfunction ?

A

UMN disease : loss of inhibition of urethral sphincter → increase urethral resistance. Often associated with other severe neuro signs, such as recumbency.

  • Skeletal m. relaxants : to inhibit striated m. of external sphincter → dantrolene or benzodiazepines (diazepam)
  • Sympatholytic drugs : to inhibit ⍺1 receptor in smooth muscle of internal sphincter → ACP
  • Parasympathomimetic drugs : to stimulate the detrusor → bethanechol
36
Q

What are the most common neurologic causes of incontinence ?

A
  • EHV-1 (rarely EHV-4) : ataxia, paresis and urinary incontinence
  • Polyneuritis equi (neuritis of the cauda equine) : start with perineal hyperesthesia (pruritus) and hypalgesia/analgesia → progressive paralysis of the tail, rectum, anus, and bladder + muscle atrophy of hindlimb (asymetric) + asymetric cranial nerve signs (dysphagia, tongue paralysis, facial, headtilt, nystagmus…)
  • Sacral / coccygeal trauma
  • EPM
  • Cervical stenotic myelopathy
  • Equine degenerative myelopathy (eNAD/EDM)
  • EMND
  • Neoplasia (rare → melanoma)
  • Idiopathic bladder paralysis
37
Q

How to differenciate bewteen cystoliths and sabulous urolithiasis ?

A

Cystoliths are usually found in small bladder, and incontinence is often accompanied by stranguria.

Sabulous urolithiasis is the accumulation of urine sediments, in the ventral aspect of a large and atonic bladder.
Idiopathic bladder paralysis → chronic distension of the bladder due to sediments accumulation → myogenic detrusor damage → perpetuates the bladder dysfunction.

38
Q

Which noninfectious disease is responsible of symmetric ataxia, hindlimb weakness, flaccid paralysis of the tail, and urinary incontinence ?

A

Toxicicites : in horses grazing pastures containing species of sorghum (Sorghum vulgare, Sorghum halepense)

39
Q

What are the most common causes of PUPD in horses ?

A
  • Chronic kidney disease
  • PPID
  • Psychogenic polydipsia (must be distinguished from diabetes insipidus)
40
Q

Definitions of PU and PD

A

Maintenance fluid requirements : 50-60 mL/kg/day (or 2-2.5 mL/kg/h)
PD > 100 mL/kg/day ∼ 10% BW (L)

Urine production : 15-30 mL/kg/day
PU > 50 mL/kg/day ∼ 5% BW (L)

41
Q

Which tubular parts are responsible of water abs° ?
NaCl abs° ?

A

Water resorption :
- proximal tubules (70%)
- descending thin limb (15%)
- collecting ducts (15%)

NaCl resorption :
- proximal tubules
- thick ascending limb
- distal convoluted tubules

42
Q

Which neuroendocrine factors are responsible of water resorption ?

A
  • ADH (vasopressin)
  • Aldosterone
  • ANP
43
Q

What are the indications and contraindications of WDT ?
When to stop the test ?

A

WDT : to distinguish between CDI or NDI and psychogenic PD
Only indicated if USG < 1.008. Contraindicated if dehydrated or azotemic (can worsen).

Test is stopped when :
1- Target USG is reached within 24h (> 1.025)
2- Horses loses > 5% BW
3- Evidence of dehydration or azotemia
4- max 48h

Persistently dilute urine (USG < 1.008) → CDI or NDI
If USG ∈ [1.008 - 1.020] → perform a MWDT

44
Q

When and how to perform a modified WDT ?

A

MWDT : required if USG ∈ [1.008 - 1.020] → to distinguish between partial CDI and long-standing psychogenic PD with medullary washout
Water is restricted to 40 mL/kg/day for 3-4 days.

Psychogenic PD can increase USG during the MWDT.

45
Q

How to distinguish between CDI and NDI ?

A

Measure of basal ADH during WDT ( increased = NDI ; decreased = CDI)
or exogenous ADH test

46
Q

What are the daily fluid requirements of horses off feed ?

A

∼ 10 mL/kg/day

47
Q

Which drugs are responsible of iatrogenic PU ?

A
  • Corticosteroids
  • ⍺2-agonists
  • Diuretics
  • Fluid therapy
48
Q

What are the endocrine causes of polyuria ?

A
  • Diabetes insipidus (DI) : central or nephrogenic
  • Diabetes mellitus (DM) : glucosuria → osmotic diuresis
  • PPID
49
Q

Is there any significant age, sex or breed effect on [SDMA] in adult horses ?

A

No significant effect of sex
Significant breed effect (but small differences)
No impact of age (between 6 months and 18 yo)

All medians were < 14 µg/dL

Symmetric dimethylarginine concentrations in healthy neonatal foals and mares
jvim 2021

50
Q

Is the SDMA concentration of newborn foals identical to that of adult horses?
Is there a link between the SDMA of the foal and mare?

A

SDMA concentration is higher in equine neonates than in adult horses, older foals and adults with acute kidney injury.
Currently SDMA cannot be used as a marker of renal dysfunction in this age group.
Consensus : SDMA is not recommended in foals less than 6 months of age because of lack of ref ranges.

No correlation between mare and foal [SDMA]°

Symmetric dimethylarginine concentrations in healthy neonatal foals and mares
jvim 2021
Serum symmetric dimethylarginine concentration in healthy neonatal Thoroughbred foals
jvim 2022

51
Q

Based on the study of symmetric dimethylarginine (SDMA) as a biomarker for renal injury in dehydrated horses, which of the following statements is TRUE?

A) SDMA concentrations were significantly correlated with both creatinine and urea concentrations at all time points.
B) SDMA concentrations at admission were significantly different among horses with varying levels of dehydration.
C) SDMA demonstrated strong prognostic value in predicting short-term outcomes, including survival.
D) The study found no correlation between SDMA and creatinine concentrations in dehydrated horses.

A

B) SDMA concentrations at admission were significantly different among horses with varying levels of dehydration.

Explanation:
- A) is incorrect because SDMA only showed a significant correlation with creatinine, not urea or other markers.
- B) is correct because SDMA concentrations varied significantly based on the level of dehydration (mild, moderate, severe).
- C) is incorrect because the study did not find significant correlations between SDMA and short-term outcomes, including survival.
- D) is incorrect because SDMA did correlate with creatinine concentrations at admission (r = 0.412, P < 0.001).

Symmetric dimethylarginine and renal function analysis in horses with dehydration
evj 2022

52
Q

What is the interaction between furosemide and NSAID ?

A

Treatment with PBZ, firocoxib and dipyrone decreases the diuretic and natriuretic effects of furosemide by 25%. Four-hour urine volume was 25% less after pre-treatment with all NSAIDs.
Though COX-2 selective NSAIDs and dipyrone might have less severe or fewer gastrointestinal adverse effects in horses, our data suggest minimal differences in effects on furosemide-induced diuresis, and possibly, risk of nephrotoxicosis.

Effects of phenylbutazone, firocoxib, and dipyrone on the diuretic response to furosemide in horses
jvim 2023

53
Q

True or false ?
The nephrotoxicity of biphosphonates is due to the concurrent administration of NSAID ?

A

False
Bisphosphonate administration, with or without concurrent NSAIDs, can be associated with AKI in horses. Serum creatinine should be monitored prior to and following bisphosphonate treatment to minimize this risk.

Further evaluation of renal function is warranted in horses that develop clinical signs of poor appetite, lethargy, or altered urination in the days following bisphosphonate treatment.

Retrospective evaluation of acute kidney injury in horses treated with nonnitrogenous bisphosphonates (2013–2020): 8 cases
Vet Emerg Crit Care 2023

54
Q

What is the usefulness of HAVCR1/KIM1 (Hepatitis A virus cell receptor 1/Kidney injury molecule 1) marker ?

A

HAVCR1/KIM1 is detectable in urine and is associated with increases in serum creatinine concentrations of >0.3 mg/dL in horses following treatment with PBZ for 7 consecutive days.
Thus, HAVCR1/KIM1 might aid in the early detection of acute kidney injury in horses.

Preliminary evaluation of hepatitis A virus cell receptor 1/kidney injury molecule 1 in healthy horses treated with phenylbutazone
Vet Emerg Crit Care 2023

55
Q

What is the definition of oliguria?

A

Urine output < 0.5 mL/kg/h

56
Q

What is the clinical significance of nephroliths in horses ?

A

The panelists consider nephroliths in horses a consequence of CKD, rather than the inciting cause.

57
Q

What is the clinical presentation of Renal Tubular Acidosis ?

A

Anorexia, lethargy, weakness, and weight loss, associated with severe hyperchloremic metabolic acidosis with a normal anion gap.

58
Q

How to manage a RTA ?

A

Initial treatment should focus on correcting metabolic acidosis by administering IV sodium bicarbonate.
Hypokalemia should be treated with potassium chloride supplementation (or oral potassium citrate); further decreases can occur during sodium bicarbonate administration.

Most horses have a favorable clinical response within 24 to 72 hours.
Duration of treatment is unpredictable, but many require treatment for months.

59
Q

What are the several types of RTA ?

A

Normal anion gap hyperchloremic metabolic acidosis
Type 1 (distal) : impaired acid secretion in collecting duct
Type 2 (proximal) : defects in the reabsorption of HCO3- of proximal tubules
Type 3 : features of both Type 1 and Type 2
Type 4 (hyperkalemic)

60
Q

What is the clinical hypothesis with neurological signs and renal failure in a horses?

A

Uremic encephalopathy

61
Q

What are the causes of severe hyponatremia in foals ?

A

Retention of free water or excess loss of sodium
- Diarrhea
- Uroperitoneum
- Renal disease
- Rhabdomyolysis
- Suspected transient pseudo-hypoaldosteronism (transient unresponsiveness of the distal tubule to the action of aldosterone due to pyelonephritis and urinary tract obstruction)
- Adrenal insufficiency
- Excessive water intake
- Iatrogenic (excessive water enemas and hypotonic fluids)

62
Q

How to manage hyponatremic encephalopathy in foals ?

A

2 approaches :
- conservative : not to exceed < 0.5 mEq/L/h
- alternative approach :
1- calculate the sodium required to initially reach a serum concentration of 120 to 125 mEq/L
2- In acute hyponatremia, this initial correction should occur rapidly to prevent further cerebral edema
3- Then the sodium required to reach a serum sodium concentration of 132 mEq/L may be provided slowly not to exceed 0.5 mEq/L/h
4- Reassess patient status and serum sodium every 4-6 h

63
Q

What is the prevalence of renal neoplasia in horses and what are the most common clinical signs?

A

The prevalence of renal neoplasia is about 1.87% in a mixed population. Common clinical signs include hematuria, ascites, stranguria.

2024 tumors of urogenital vet clinic

64
Q

What is the most common clinical sign of bladder neoplasia in horses and what are the main diagnostic methods and treatment?

A

The most common clinical sign of bladder neoplasia in horses is hematuria. The main diagnostic methods are ultrasound and cystoscopy. Successful treatment was reported following surgical debulking and piroxicam therapy in a case of transitional cell carcinoma

2024 tumors of urogenital vet clinic

65
Q

What is the most common type of neoplasia affecting the penis and prepuce in horses, and what are the main treatment options?

A

The most common type is squamous cell carcinoma. Main treatment options include surgical resection (various techniques) and topical chemotherapy for early lesions. 64.5-87.5% survival without recurrence depending on treatment

2024 tumors of urogenital vet clinic

66
Q

How is testicular neoplasia typically diagnosed and treated in horses?

A

Testicular neoplasia is typically diagnosed using ultrasound and biopsy. The standard treatment is orchidectomy of the affected testicle

2024 tumors of urogenital vet clinic

67
Q

What are the main treatment options for vulvar and vaginal neoplasia in mares?

A

The main treatment options for vulvar and vaginal neoplasia in mares include surgical excision, laser resection, and topical chemotherapy for early lesions.

2024 tumors of urogenital vet clinic

68
Q

What are the typical clinical signs of uterine neoplasia in mares and how is it diagnosed?

A

Typical clinical signs of uterine neoplasia in mares include infertility, abdominal pain, and bloody vulvar discharge.

It is diagnosed using rectal ultrasound, hysteroscopy, and biopsy

2024 tumors of urogenital vet clinic

69
Q

What is the most common type of ovarian neoplasia in mares and what are the typical behavioral changes associated with it?

A

The most common type of ovarian neoplasia in mares is granulosa cell tumor. Typical behavioral changes include stallion-like behavior>aggression>prolonged estrus> anestrus.

2024 tumors of urogenital vet clinic

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