Renal/Urinary Flashcards
(280 cards)
2
Q
Weese et al. (2019): What are the four categories of UTIs defined in the ISCAID guidelines?
A
Sporadic bacterial cystitis, recurrent bacterial cystitis, pyelonephritis, and subclinical bacteriuria.
3
Q
Weese et al. (2019): What defines a ‘sporadic bacterial cystitis’?
A
Clinical signs of lower urinary tract disease in an otherwise healthy animal, with infrequent history of prior UTIs.
4
Q
Weese et al. (2019): How is ‘recurrent bacterial cystitis’ defined?
A
≥3 episodes of bacterial cystitis within 12 months, or ≥2 episodes within 6 months.
5
Q
Weese et al. (2019): What is ‘subclinical bacteriuria’?
A
Positive urine culture in the absence of clinical signs of UTI.
6
Q
Weese et al. (2019): When is treatment indicated for subclinical bacteriuria?
A
Only in specific cases (e.g., prior to urogenital surgery, or in immunocompromised patients).
7
Q
Weese et al. (2019): What is the first-line diagnostic recommendation for suspected UTI?
A
Cystocentesis urine sample for urinalysis and quantitative aerobic culture.
8
Q
Weese et al. (2019): Which antimicrobials are recommended for empiric treatment of sporadic cystitis in dogs?
A
Amoxicillin or trimethoprim-sulfonamide for 3–5 days.
9
Q
Weese et al. (2019): Why is amoxicillin–clavulanate not first-line for uncomplicated cystitis?
A
Broader spectrum than needed; use reserved for resistant or more complicated cases.
10
Q
Weese et al. (2019): What is the role of culture in monitoring treatment response for sporadic cystitis?
A
Not routinely recommended unless clinical signs persist or recur.
11
Q
Weese et al. (2019): What pharmacokinetic/pharmacodynamic principle supports using short-duration antimicrobials in UTIs?
A
Time > MIC is easily achieved in urine due to high urinary drug concentrations, supporting short-course efficacy.
12
Q
Weese et al. (2019): What is the physiological basis for bacteriuria without clinical signs?
A
The urinary tract’s mucosal defenses and immune surveillance may limit host inflammatory responses, allowing bacterial colonization without overt infection (subclinical bacteriuria).
13
Q
Weese et al. (2019): What are two physiological reasons cats are more prone to subclinical bacteriuria?
A
Reduced urine concentrating ability in CKD and age-associated immune dysregulation.
14
Q
Weese et al. (2019): Why is cystocentesis the preferred urine collection method for culture?
A
Minimizes contamination from urethral/genital flora, improving diagnostic specificity for true infection.
15
Q
Weese et al. (2019): What host factors increase risk of UTI progression to pyelonephritis?
A
Vesicoureteral reflux, ureteral obstruction, immunosuppression, and diabetes mellitus.
16
Q
Weese et al. (2019): What is the pathophysiologic consequence of ascending infection to the kidney?
A
Pyelonephritis can cause interstitial nephritis, tubular damage, and systemic inflammatory response with or without azotemia.
17
Q
Weese et al. (2019): What is the rationale for avoiding empiric fluoroquinolone use in uncomplicated UTI?
A
Risk of promoting antimicrobial resistance; fluoroquinolones are critically important drugs that should be reserved for more serious infections.
18
Q
Weese et al. (2019): How is antimicrobial resistance influenced by over-treatment of subclinical bacteriuria?
A
Unnecessary antibiotic exposure selects for resistant organisms without clinical benefit.
19
Q
Weese et al. (2019): What bacterial resistance mechanisms are commonly encountered in recurrent UTIs?
A
Extended-spectrum beta-lactamases (ESBLs), efflux pumps, and biofilm formation.
20
Q
Weese et al. (2019): What is the recommended approach if multidrug-resistant bacteria are cultured?
A
Base treatment on susceptibility testing and consider consultation with infectious disease specialists; avoid empiric escalation.
21
Q
Weese et al. (2019): What are key stewardship principles emphasized in the guidelines?
A
Minimize antibiotic use, use narrow-spectrum agents, avoid unnecessary treatment, and use short courses when appropriate.
22
Q
Taylor et al. (2025): What are the most common clinical signs associated with FLUTD in cats?
A
Dysuria, pollakiuria, hematuria, periuria, and stranguria.
23
Q
Taylor et al. (2025): What are the main differentials for FLUTD in cats?
A
Feline idiopathic cystitis (FIC), urolithiasis, urethral plugs, bacterial UTI, neoplasia, and anatomical defects.
24
Q
Taylor et al. (2025): What is the most common cause of FLUTD in cats under 10 years old?
A
Feline idiopathic cystitis (FIC).
25
Q
Taylor et al. (2025): What diagnostics are recommended for a first-time, non-obstructive FLUTD episode in a young adult cat?
A
Minimum database (UA, sediment exam), +/- abdominal radiographs, and behavioral/environmental assessment.
26
Taylor et al. (2025): What is the cornerstone of management for FIC?
Multimodal environmental modification (MEMO) and analgesia.
27
Taylor et al. (2025): What analgesics are recommended for managing acute FLUTD pain?
Buprenorphine or NSAIDs (with caution depending on renal status).
28
Taylor et al. (2025): When is antibiotic therapy indicated in FLUTD?
Only with confirmed bacterial UTI based on urine culture. Not indicated for FIC or urethral plugs.
29
Taylor et al. (2025): What environmental interventions are considered part of MEMO?
Increasing litter box number/access, decreasing stressors, increasing play/enrichment, and improving owner-cat interaction.
30
Taylor et al. (2025): How many litter boxes are recommended for indoor cats in MEMO?
One per cat, plus one extra (N+1 rule).
31
Taylor et al. (2025): What clinical signs or features should prompt concern for urethral obstruction in male cats?
Straining to urinate with no urine production, vocalizing, firm bladder on palpation, and systemic signs like vomiting or collapse.
32
What is the most common cause of feline lower urinary tract signs (FLUTS) in cats under 10 years old, according to the 2025 iCatCare guidelines?
Feline Idiopathic Cystitis (FIC).
33
What are the core pathophysiologic factors thought to underlie FIC?
Stress-induced neurohormonal dysregulation, altered urothelial permeability, and increased sympathetic drive.
34
What diagnostic approach is recommended to differentiate FIC from other causes of FLUTS?
History, physical exam, urinalysis, and imaging (radiography ± ultrasound); culture if infection is suspected.
35
What is the role of urinalysis in the workup of feline LUTD per 2025 guidelines?
To identify hematuria, pyuria, crystalluria, urine pH, and specific gravity; helps distinguish infection from sterile cystitis.
36
When should a urine culture be performed?
In male cats, cats with systemic illness, recurrent signs, or pyuria/bacteriuria seen on urinalysis.
37
What dietary strategy is recommended for cats with recurrent FIC?
Increased water intake via wet food, addition of water to food, and use of therapeutic urinary diets formulated to reduce crystalluria and urine concentration.
38
What environmental strategy is emphasized in long-term FIC management?
Multimodal Environmental Modification (MEMO), including enrichment, litterbox management, and stress reduction.
39
How is urethral obstruction in male cats managed acutely?
Emergency stabilization, catheterization to relieve obstruction, IV fluids, analgesia, and monitoring for post-obstructive diuresis.
40
What pharmacologic agents are recommended for acute FIC flares?
Analgesics (e.g., buprenorphine), anxiolytics (e.g., gabapentin or trazodone), and sometimes short-term alpha antagonists or antispasmodics.
41
What recurrence prevention measures are supported in the guidelines?
Diet modification, MEMO, regular water intake, weight control, and managing stress triggers (e.g., changes in household routine).
42
When is antibiotic use indicated for cats with FLUTS?
Only if there is documented bacterial infection by culture and sensitivity; not recommended empirically in FIC cases.
43
What is the recommended minimum urine specific gravity (USG) goal to reduce FIC recurrence?
< 1.035, ideally closer to 1.020–1.030 to ensure dilute urine.
44
What is the role of glucosaminoglycan (GAG) supplementation in feline LUTD?
May have benefit in some cases of FIC by improving urothelial barrier function, but evidence is limited.
45
What is the definition of recurrent FIC per the 2025 guidelines?
Three or more episodes within 12 months.
46
Which population of cats is most at risk for FIC?
Young to middle-aged, overweight, indoor-only, neutered male cats with a history of stress or environmental change.
47
According to Taylor et al. (2025), what is the proposed primary pathophysiologic mechanism driving FIC?
A neurogenic inflammatory response initiated by stress, resulting in exaggerated sympathetic nervous system activity and altered bladder afferent signaling.
48
How does the sympathetic nervous system contribute to bladder dysfunction in FIC cats?
Cats with FIC have increased systemic and local sympathetic tone, leading to vasoconstriction, ischemia, and sensitization of bladder afferents.
49
What neuroendocrine abnormalities are implicated in FIC pathogenesis?
Inappropriate hypothalamic-pituitary-adrenal (HPA) axis responses to stress with reduced cortisol production, impairing the cat's ability to buffer stress.
50
What structural bladder wall changes are observed in FIC according to the 2025 guidelines?
Disruption of the glycosaminoglycan (GAG) layer, increased permeability of the urothelium, and submucosal edema or hemorrhage.
51
What is the role of urothelial barrier dysfunction in FIC?
Loss of GAGs and tight junction integrity permits urinary solutes (e.g., K⁺, H⁺, irritants) to penetrate deeper layers, triggering inflammation and pain.
52
What role does neurogenic inflammation play in the bladder of cats with FIC?
Stimulation of C-fiber afferents leads to substance P and CGRP release, causing mast cell degranulation and nociceptor sensitization, sustaining pain and inflammation.
53
How is central sensitization thought to contribute to chronic FIC signs?
Prolonged afferent input from the bladder leads to heightened CNS responsiveness (central sensitization), resulting in allodynia and hyperalgesia.
54
How is FIC considered a systemic syndrome rather than just a bladder disease?
Evidence of stress axis dysregulation, systemic sympathetic overactivity, and comorbidities like GI or dermatologic hypersensitivity suggest a global neuroendocrine-immune dysfunction.
55
What parallels are drawn between FIC and human interstitial cystitis/bladder pain syndrome (IC/BPS)?
Both involve stress-exacerbated chronic pelvic pain, sensory nerve upregulation, urothelial barrier defects, and abnormal neuroimmune signaling.
56
Ross 2022: What is the pathophysiologic progression of AKI?
AKI progresses from initiation (insult), extension (hypoxia/inflammation), maintenance (tubular dysfunction), to recovery (repair or fibrosis).
57
Ross 2022: What cellular changes occur during AKI?
Tubular epithelial cells lose polarity, detach, die (apoptosis/necrosis), and slough, causing obstruction, backleak, and inflammation.
58
Ross 2022: What are the major causes of AKI in dogs and cats?
Ischemia, toxins (e.g., ethylene glycol, aminoglycosides), infections (e.g., leptospirosis, pyelonephritis), and systemic disease (e.g., pancreatitis).
59
Ross 2022: How is AKI diagnosed?
Based on azotemia, oliguria/anuria, and clinical history. Confirmed by increasing creatinine, imaging (renal size, echogenicity), and urinalysis.
60
Ross 2022: What biomarkers are used in AKI diagnosis beyond creatinine?
SDMA, NGAL, cystatin C, urinary GGT/creatinine ratio, and KIM-1 are under investigation for early detection.
61
Ross 2022: What is the KDIGO staging system and its relevance to veterinary AKI?
KDIGO stages AKI by serum creatinine and urine output. Although not fully validated in animals, it provides a useful severity framework.
62
Ross 2022: What is the goal of fluid therapy in AKI?
Restore perfusion, correct dehydration, avoid overload. Use isotonic crystalloids; monitor for fluid responsiveness and renal output.
63
Ross 2022: What strategies minimize nephrotoxicity in AKI patients?
Avoid nephrotoxic drugs, ensure euvolemia, dose drugs based on renal clearance, and monitor drug levels when possible.
64
Ross 2022: When is renal replacement therapy (RRT) indicated in AKI?
Severe oliguria/anuria, hyperkalemia, volume overload, uremia, and worsening azotemia despite medical therapy.
65
Ross 2022: What are the prognostic indicators in AKI?
Etiology, severity of azotemia, oliguria, presence of systemic illness, and response to treatment affect prognosis.
66
Ross 2022: What are common complications of AKI?
Hyperkalemia, volume overload, acidosis, uremic gastritis, arrhythmias, and secondary infections.
67
Ross 2022: What is the pathophysiologic role of inflammation in AKI?
Ischemia/reperfusion triggers DAMPs → TLR activation → cytokine/chemokine release → neutrophil infiltration → more tubular injury.
68
Ross 2022: What histologic findings are typical in AKI?
Acute tubular necrosis, tubular dilation, cellular debris, loss of brush border, and interstitial inflammation.
69
Ross 2022: What is the role of oxidative stress in AKI?
ROS generated during reperfusion or by activated neutrophils damage cell membranes, proteins, and DNA, worsening injury.
70
According to Ross 2022, what are the main causes of AKI in dogs and cats?
Ischemia, nephrotoxins (e.g., NSAIDs, aminoglycosides, ethylene glycol), infectious diseases (e.g., leptospirosis, pyelonephritis), and systemic illness (e.g., pancreatitis, sepsis).
71
In Ross 2022, how is AKI staged in veterinary medicine?
Using the IRIS staging system, which categorizes AKI into Grades I–V based on serum creatinine, urine output, and clinical signs.
72
What are key clinical signs of AKI as noted in Ross 2022?
Anorexia, vomiting, lethargy, polyuria/oliguria/anuria, dehydration, and uremic halitosis.
73
What diagnostic tests are emphasized by Ross 2022 for AKI workup?
Serum chemistry, CBC, urinalysis (including UPC), imaging (ultrasound), infectious disease testing (e.g., leptospirosis PCR), and urine culture.
74
What are the hallmark urinalysis findings in AKI per Ross 2022?
Isosthenuria (USG 1.008–1.012), proteinuria, glucosuria (without hyperglycemia), and presence of casts.
75
How does Ross 2022 define the phases of AKI pathophysiology?
1. Initiation 2. Extension 3. Maintenance 4. Recovery.
76
What is the significance of the “extension” phase in Ross 2022?
It includes ongoing hypoxia and inflammation that perpetuate tubular damage, often a therapeutic target window.
77
What therapies are outlined by Ross 2022 for managing AKI?
IV fluid therapy (resuscitation and diuresis), antiemetics, gastroprotectants, blood pressure support, and addressing underlying cause.
78
What complications of AKI are discussed in Ross 2022?
Hyperkalemia, volume overload, metabolic acidosis, anemia, uremic toxins, and hypertension.
79
According to Ross 2022, how is volume overload recognized?
Sudden weight gain, serous nasal discharge, chemosis, pulmonary crackles, pleural effusion, and ascites.
80
What is the role of renal replacement therapy (RRT) per Ross 2022?
Indicated for severe AKI cases with oliguria/anuria, refractory hyperkalemia, or uremia; includes intermittent hemodialysis and CRRT.
81
What prognostic factors are associated with poor outcome per Ross 2022?
Oliguria, high creatinine at presentation, presence of systemic illness (e.g., sepsis), and lack of improvement over 48–72 hours.
82
What is the role of diuretics in AKI according to Ross 2022?
They may help convert oliguric to non-oliguric AKI, but do not improve survival; furosemide challenge can be used diagnostically.
83
What preventive strategies for AKI are discussed by Ross 2022?
Avoid nephrotoxins, early fluid therapy in hypoperfused patients, appropriate anesthetic monitoring, and careful drug dosing.
84
How does Ross 2022 address use of biomarkers for AKI?
Discusses neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, and SDMA as potential early markers of kidney injury.
85
According to Brown et al. (2015), what was the primary objective of the study?
To evaluate GFR, urine production, and fractional clearance of electrolytes in dogs with AKI and assess their association with survival.
86
How was glomerular filtration rate (GFR) measured in this study by Brown et al. (2015)?
GFR was measured using iohexol plasma clearance.
87
What was the most important predictor of survival in dogs with AKI, according to Brown et al. (2015)?
Higher GFR was significantly associated with survival.
88
What urine production threshold was associated with better survival outcomes in Brown et al. (2015)?
Urine output >1 mL/kg/h was associated with a higher survival rate.
89
What fractional clearance (FC) value was found to be most elevated in non-survivors?
FC of sodium (FCNa) was significantly higher in non-survivors.
90
What is fractional clearance of sodium (FCNa), and how is it calculated?
FCNa = (Urine Na × Plasma Cr) / (Plasma Na × Urine Cr) × 100. It estimates the percentage of filtered sodium excreted.
91
According to Brown et al. (2015), what does a high FCNa suggest in AKI pathophysiology?
Impaired tubular reabsorption, indicating more severe tubular injury.
92
How did non-survivors differ in GFR compared to survivors in the Brown et al. (2015) study?
Non-survivors had significantly lower GFRs.
93
How do the authors interpret the relationship between oliguria and survival in dogs with AKI?
Oliguria (<1 mL/kg/h) was a negative prognostic indicator for survival.
94
What is the physiologic mechanism linking low GFR to increased FCNa in AKI?
Tubular damage impairs Na reabsorption, and low GFR reduces filtered load, amplifying fractional excretion.
95
What are input sensors involved in renal sodium handling during AKI?
Macula densa sodium sensors and intrarenal baroreceptors detect decreased Na delivery and perfusion pressure.
96
What is the 'controller algorithm' for sodium retention in AKI physiology?
The RAAS system adjusts Na reabsorption through aldosterone signaling in the distal tubule and collecting duct.
97
What are the 'actuators' responsible for sodium reabsorption in the kidney?
Na+/K+ ATPase pumps, ENaC channels, and Na+/H+ exchangers in tubular epithelium.
98
According to Brown et al. (2015), what was the relationship between FC of urea and survival?
FCurea was not significantly associated with survival.
99
How does decreased GFR in AKI affect systemic electrolyte balance?
Leads to hyperkalemia, hyperphosphatemia, hyponatremia due to impaired filtration and altered tubular handling.
100
How does FCNa differ from urine Na concentration as a diagnostic tool in AKI?
FCNa corrects for urine concentration and provides a more accurate index of tubular function.
101
Why is iohexol clearance a reliable marker of GFR according to Brown et al. (2015)?
It is freely filtered, not secreted or reabsorbed, and provides a direct measurement of GFR.
102
What is the clinical significance of measuring urine output in AKI?
It helps identify oliguria or anuria, guides fluid therapy, and serves as a non-invasive prognostic marker.
103
What electrolyte FC values were most useful in distinguishing survivors from non-survivors in AKI?
FCNa and FCCl were most predictive of survival outcomes.
104
How might these findings influence ECC management of AKI in dogs?
Emphasizes early monitoring of GFR, urine output, and FCNa to guide prognosis and therapy decisions.
105
According to Cooper (2015), what is the most common pathophysiologic cause of feline urethral obstruction (UO)?
Urethral plugs composed of matrix and struvite crystals are the most common cause, often due to functional or idiopathic urethral spasm/inflammation.
106
What electrolyte and acid-base abnormalities are classically associated with feline UO per Cooper (2015)?
Hyperkalemia, hyperphosphatemia, metabolic acidosis, and azotemia.
107
According to Cooper (2015), why is rapid decompression of the bladder not always ideal?
Rapid decompression can cause post-obstructive diuresis and hypovolemia if not carefully managed.
108
What are the primary controversies outlined by Cooper (2015) in UO management?
Use of decompressive cystocentesis, timing and technique of catheterization, duration of hospitalization, sedation protocols, and surgical interventions like PU.
109
What is decompressive cystocentesis, and what are the proposed benefits?
It is percutaneous bladder decompression using a needle; it may stabilize hyperkalemia and improve cardiovascular function before catheterization.
110
According to Cooper (2015), what are risks of decompressive cystocentesis in UO cats?
Potential for uroabdomen, especially if the bladder is friable or trauma occurs during the procedure.
111
What role does IV fluid therapy serve before and after catheterization in obstructed cats?
Restores perfusion, corrects electrolyte derangements, supports diuresis, and minimizes post-obstructive complications.
112
How does alpha-1 adrenergic antagonism play a role in UO treatment?
Drugs like prazosin relax urethral smooth muscle, reducing functional obstruction from spasm.
113
What is post-obstructive diuresis, and why is it clinically important?
Excessive urine output after relief of obstruction; it can lead to dehydration, hypovolemia, and electrolyte losses.
114
What are Cooper's (2015) recommendations regarding the duration of catheterization?
Shorter duration may reduce hospitalization and cost, but risk of re-obstruction must be weighed; 24–48 hours is commonly cited.
115
What 'input sensors' initiate the physiologic response to obstruction?
Bladder wall stretch receptors, renal baroreceptors, and chemoreceptors detecting uremic toxin accumulation.
116
What 'controller algorithm' adjusts physiologic responses to UO?
Neurohormonal signaling (RAAS, ADH), baroreflex activation, and local inflammatory pathways adjust renal perfusion and bladder function.
117
What are the 'actuators' in UO recovery post-catheterization?
Diuresis (via ADH downregulation), vasodilation (RAAS suppression), bladder contractility, and urethral relaxation.
118
How does hyperkalemia in feline UO contribute to bradyarrhythmias?
High K+ causes membrane depolarization, reducing myocardial excitability and conduction velocity, leading to AV block or asystole.
119
According to Cooper (2015), what is the role of calcium gluconate in UO treatment?
Stabilizes the myocardium in severe hyperkalemia but does not reduce potassium levels.
120
What is the mechanism of action of insulin/dextrose therapy in hyperkalemia?
Insulin promotes cellular K+ uptake; dextrose prevents hypoglycemia.
121
What clinical sign may indicate severe bladder rupture or uroabdomen in obstructed cats?
Progressive abdominal distension, worsening azotemia despite catheterization, and free abdominal fluid with creatinine >2x serum.
122
What are the long-term management strategies discussed by Cooper (2015) to reduce recurrence?
Dietary modification, environmental enrichment, stress reduction, and potential use of PU in recurrent obstructions.
123
What factors should influence the decision to perform perineal urethrostomy (PU)?
Frequency of obstruction, urethral damage or stricture, owner resources, and failure of medical management.
124
What does Cooper (2015) suggest about early discharge with indwelling catheters in stable patients?
May be appropriate with careful monitoring and client education; could reduce hospital burden and cost.
125
According to Harison et al. (2012), what was the main objective of the study?
To determine whether the degree of acute azotemia at hospital admission could predict survival in dogs and cats.
126
What criteria were used to define acute azotemia in this study by Harison et al. (2012)?
Elevated serum creatinine concentration above the reference interval in a previously non-azotemic patient, with compatible clinical signs of acute onset.
127
What was the primary outcome measured in Harison et al. (2012)?
Survival to hospital discharge.
128
What was the significant finding regarding the relationship between serum creatinine and mortality?
Increasing serum creatinine concentration at admission was significantly associated with increased mortality in both species.
129
What creatinine cutoff was associated with the highest mortality rate in cats according to Harison et al. (2012)?
Cats with serum creatinine ≥10 mg/dL had significantly higher mortality rates.
130
How did the presence of anuria or oliguria affect survival according to Harison et al. (2012)?
Anuric or oliguric patients had significantly lower survival rates than those with normal or polyuric urine output.
131
How does azotemia lead to systemic clinical signs in AKI patients?
Accumulation of uremic toxins affects neurologic, GI, and cardiovascular systems; also disrupts electrolyte and acid-base homeostasis.
132
What are some complications of severe azotemia identified in this study?
Hyperkalemia, metabolic acidosis, vomiting, seizures, and hypothermia.
133
According to Harison et al. (2012), was species (dog vs. cat) a significant predictor of outcome?
No significant difference in survival was found between dogs and cats after adjusting for azotemia severity.
134
How does elevated serum creatinine reflect glomerular filtration rate (GFR)?
Serum creatinine rises as GFR declines, typically becoming elevated after ~75% reduction in functional nephrons.
135
What are the 'input sensors' in renal azotemia physiology?
Juxtaglomerular apparatus detects decreased perfusion; macula densa senses tubular sodium and flow.
136
What is the 'controller algorithm' for compensatory response to acute azotemia?
Activation of RAAS, sympathetic nervous system, and vasopressin secretion to conserve volume and maintain perfusion.
137
What are the 'actuators' in response to azotemia?
Renin release, aldosterone-driven sodium retention, vasoconstriction, and ADH-mediated water reabsorption.
138
Why is urine output a critical clinical variable in AKI prognosis per Harison et al. (2012)?
Oliguria/anuria reflects more severe tubular damage and decreased renal perfusion, correlating with worse outcomes.
139
What is the clinical utility of serial creatinine measurements in AKI management?
Trending creatinine helps assess recovery or progression and guides fluid and electrolyte therapy.
140
Why might early identification of azotemia not always correlate with survival outcome?
Survival also depends on reversibility of the underlying cause, presence of comorbidities, and supportive care quality.
141
What is the role of fluid therapy in reversing pre-renal azotemia?
Restores renal perfusion and may normalize GFR if structural injury hasn't occurred.
142
How does dehydration contribute to azotemia pathophysiologically?
Hypovolemia decreases renal perfusion, reducing GFR and promoting reabsorption of nitrogenous wastes.
143
What limitations did Harison et al. (2012) acknowledge in their study?
Retrospective design, lack of consistent diagnostic criteria across cases, and absence of long-term follow-up.
144
What is a clinical implication of this study for ECC practice?
Admission creatinine is a strong prognostic marker; patients with severe azotemia and oliguria need more aggressive monitoring and care.
145
According to Keir & Kellum (2015), what is the pathophysiology of acute kidney injury (AKI) in sepsis?
AKI in sepsis is multifactorial, involving inflammation, microvascular dysfunction, mitochondrial injury, and dysregulated immune responses, rather than solely ischemia.
146
What is the role of renal microcirculation in septic AKI, as described by Keir & Kellum (2015)?
Sepsis causes heterogeneous perfusion, microthrombi, and endothelial dysfunction, leading to regional hypoxia despite preserved or increased total renal blood flow.
147
According to Keir & Kellum (2015), how does mitochondrial dysfunction contribute to septic AKI?
Impaired mitochondrial respiration in renal tubular cells reduces ATP production, leading to cell injury and apoptosis, even in the absence of overt hypoperfusion.
148
What is the significance of tubular cell apoptosis in septic AKI?
Tubular cell apoptosis leads to loss of reabsorptive capacity and structural integrity, contributing to functional decline in GFR.
149
How does the systemic inflammatory response contribute to AKI in sepsis?
Pro-inflammatory cytokines (e.g., TNF-α, IL-6) and DAMPs activate renal endothelium and immune cells, promoting oxidative stress, permeability, and injury.
150
What are the clinical criteria for diagnosing AKI in sepsis according to Keir & Kellum (2015)?
Increased serum creatinine or decreased urine output over a defined period, often per AKIN or KDIGO criteria.
151
Why is serum creatinine an unreliable early marker of septic AKI?
Creatinine rises late, is affected by muscle mass and dilutional factors, and may not reflect acute tubular injury immediately.
152
What are potential early biomarkers of septic AKI discussed in Keir & Kellum (2015)?
NGAL (neutrophil gelatinase-associated lipocalin), KIM-1, and IL-18 may identify injury before creatinine rises.
153
According to Keir & Kellum (2015), what is the goal of fluid resuscitation in septic AKI?
To restore effective circulating volume and renal perfusion without inducing fluid overload.
154
What is the risk of excessive fluid therapy in septic AKI?
Fluid overload can worsen renal congestion, impair oxygen delivery, and contribute to poor outcomes.
155
What vasopressor is recommended for septic AKI according to Keir & Kellum (2015)?
Norepinephrine is first-line due to its efficacy in raising MAP with minimal renal vasoconstriction.
156
What is the physiologic target mean arterial pressure (MAP) in managing septic AKI?
Generally, MAP ≥65 mmHg is recommended to ensure renal perfusion, though individualized targets may vary.
157
How does Keir & Kellum (2015) describe the role of renal replacement therapy (RRT) in septic AKI?
RRT is used when fluid, electrolyte, or acid-base imbalances become life-threatening or refractory to medical management.
158
What are the ‘input sensors’ involved in septic AKI?
Renal endothelial cells, Toll-like receptors (e.g., TLR4), and tubular cells detect PAMPs and DAMPs to initiate inflammation.
159
What is the ‘controller algorithm’ that governs AKI progression in sepsis?
The integration of cytokine signaling (e.g., IL-6, TNF-α), ROS production, and metabolic shutdown drives injury and repair balance.
160
What are the 'actuators' in the septic kidney?
Endothelial activation, tubular apoptosis, immune cell infiltration, mitochondrial dysfunction, and microvascular thrombosis.
161
How do DAMPs and PAMPs contribute to kidney injury in sepsis?
They activate pattern recognition receptors (PRRs), triggering NF-κB pathways and cytokine release, promoting inflammation and damage.
162
Why might AKI occur in septic patients despite preserved systemic perfusion?
Due to intrarenal perfusion heterogeneity, inflammation, and cellular injury not detectable via global hemodynamics.
163
What is the role of tight glycemic control in septic AKI prevention per Keir & Kellum (2015)?
Avoidance of severe hyperglycemia is beneficial, but aggressive glucose control increases risk of hypoglycemia and is not uniformly recommended.
164
What is the clinical implication of this paper for ECC practice?
Early recognition of septic AKI, avoidance of fluid overload, and support of mitochondrial and microvascular function are key to improving outcomes.
165
What was the objective of the study by Sigrist et al. (2017) on HES in cats?
To evaluate the effects of 6% hydroxyethyl starch (HES) 130/0.4 administration on serum creatinine and the development of AKI in nonazotemic cats.
166
What type of study was conducted by Sigrist et al. (2017)?
A prospective, randomized, blinded clinical trial.
167
What dose of HES was administered to the treatment group in Sigrist et al. (2017)?
2 mL/kg IV bolus followed by 2 mL/kg/h for 5 hours.
168
According to Sigrist et al. (2017), did HES administration lead to increased creatinine levels or AKI in cats?
No statistically significant increase in serum creatinine or incidence of AKI was observed within 96 hours.
169
What was the control fluid used in the study by Sigrist et al. (2017)?
Isotonic crystalloid solution (e.g., balanced electrolyte solution).
170
What criteria were used to define AKI in this study?
An increase in serum creatinine of ≥26 μmol/L (0.3 mg/dL) within 48 hours.
171
How does HES potentially cause AKI in other species according to cited literature?
HES may accumulate in renal tubular cells, causing osmotic nephrosis-like lesions, inflammation, and impaired GFR.
172
What is the significance of this study in the context of the broader HES controversy?
It provides preliminary evidence that short-term, low-dose HES 130/0.4 may not induce AKI in nonazotemic cats, but larger studies are needed.
173
What are the proposed mechanisms of HES-induced renal injury?
Tubular vacuolization, lysosomal rupture, inflammation, increased interstitial pressure, and altered osmotic gradients.
174
What are the 'input sensors' involved in detecting renal stress following colloid administration?
Tubular epithelial cells and the renal interstitium respond to osmotic stress and intracellular HES accumulation.
175
What is the 'controller algorithm' in the kidney's response to colloid-induced injury?
Cytokine signaling, ROS generation, and autophagy or apoptosis pathways regulate renal repair or injury progression.
176
What are the 'actuators' that mediate renal damage in colloid nephropathy?
Infiltration of inflammatory cells, cellular swelling, lysosomal rupture, and tubular dysfunction.
177
How does colloid oncotic pressure potentially affect GFR in fluid therapy?
High oncotic pressure may reduce glomerular ultrafiltration pressure and impair GFR, particularly in hypoperfused kidneys.
178
According to Sigrist et al. (2017), is monitoring creatinine sufficient to rule out HES nephrotoxicity?
Not definitively; subclinical injury may occur, and biomarkers or histopathology would provide more sensitive detection.
179
What key limitation did the authors acknowledge in Sigrist et al. (2017)?
Small sample size and short duration of monitoring may underestimate subacute or delayed renal injury.
180
What is the clinical implication of this study for ECC use of HES in cats?
Cautious, low-dose HES use in nonazotemic cats appears not to acutely worsen renal parameters, but further evidence is needed before routine use.
181
What safety conclusion can be drawn from Sigrist et al. (2017) regarding HES 130/0.4?
It did not significantly increase serum creatinine or AKI incidence within the monitored timeframe.
182
How is HES 130/0.4 structurally different from older HES formulations?
Lower molecular weight and lower molar substitution, which theoretically reduces tissue accumulation and nephrotoxicity.
183
What is osmotic nephrosis, and how is it relevant to HES administration?
A histological lesion characterized by tubular cell swelling and vacuolization, associated with accumulation of starch molecules like HES.
184
In ECC practice, what patient populations might still be at risk from HES use despite this study?
Patients with preexisting azotemia, shock-induced AKI, or sepsis may be more vulnerable to HES-induced renal injury.
185
According to Sykes et al. (2023), what are the two most common organ systems affected in canine leptospirosis?
The kidneys (tubulointerstitial nephritis → AKI) and liver (cholestatic hepatopathy) are most commonly affected.
186
What is the most common route of infection for Leptospira in dogs?
Through mucous membranes or abraded skin exposed to contaminated water or soil, especially from the urine of infected reservoir hosts.
187
What is the primary reservoir host for canine leptospirosis globally according to Sykes et al. (2023)?
Rodents, especially Rattus norvegicus, are the most important reservoir hosts worldwide.
188
What renal pathophysiology defines leptospirosis-associated AKI?
Acute tubulointerstitial nephritis, tubular dysfunction (e.g., glucosuria, isosthenuria), and proteinuria from both tubular and glomerular injury.
189
What are hallmark clinicopathologic features of canine leptospirosis-induced AKI?
Azotemia, isosthenuria or hyposthenuria, glucosuria with normoglycemia, proteinuria, pyuria, and granular casts.
190
What is leptospiral pulmonary hemorrhage syndrome (LPHS) and its prognosis?
LPHS is a severe manifestation involving alveolar hemorrhage; it carries a high mortality rate (up to 70%).
191
How does Leptospira evade the host immune system early in infection?
Via corkscrew motility, biofilm formation, endothelial barrier disruption, and avoidance of innate immune recognition through LPS variation.
192
What does the 2023 consensus say about cats and leptospirosis?
Cats are relatively resistant to clinical disease but may act as subclinical carriers and should be included in One Health considerations.
193
According to the 2023 consensus, what are the most sensitive diagnostic strategies for leptospirosis?
A combination of NAAT (PCR) and serologic testing (MAT), ideally using paired titers and multiple serovars.
194
What is the MAT titer threshold considered supportive of leptospirosis in dogs?
A single MAT titer ≥1:800 is considered supportive; a 4-fold rise between acute and convalescent samples is confirmatory.
195
What are 'input sensors' in the immune detection of Leptospira?
TLRs (especially TLR2 and TLR4) on renal tubular and immune cells detect leptospiral LPS and DAMPs.
196
What is the 'controller algorithm' in the immune response to leptospirosis?
Activation of innate immune pathways, NF-κB signaling, neutrophil chemotaxis, and release of inflammatory cytokines like IL-6, TNF-α.
197
What are the 'actuators' that mediate clinical disease in leptospirosis?
Platelet dysfunction, endothelial damage, tubular apoptosis, pulmonary capillary leak, and cytokine-driven systemic inflammation.
198
How does leptospirosis-associated coagulopathy manifest on testing?
Thrombocytopenia, prolonged PT/aPTT, increased D-dimers, hypofibrinogenemia or hyperfibrinogenemia, and low antithrombin.
199
What fluid therapy recommendation is made for dogs with leptospirosis and concurrent LPHS?
Use judicious fluid therapy to avoid fluid overload; consider imaging to monitor pulmonary changes.
200
What antibiotic therapy is recommended for dogs with leptospirosis?
Doxycycline 5 mg/kg PO q12h for 14 days; if not tolerated initially, start with IV penicillin derivatives (ampicillin or penicillin G).
201
When should dialysis be considered in dogs with leptospirosis?
In IRIS AKI Grade IV dogs with creatinine >5 mg/dL, especially with hyperkalemia, anuria, or fluid overload.
202
What prognostic marker is strongly associated with non-survival in canine leptospirosis?
Serum bilirubin ≥0.6 mg/dL is associated with significantly increased risk of death (OR 16.4).
203
What are common electrolyte abnormalities in leptospirosis?
Hyponatremia, hypochloremia, hypokalemia (especially with tubular injury), or hyperkalemia (with oliguric AKI).
204
How should dogs be monitored during hospitalization for leptospirosis?
Daily biochemistry, CBC every 48h, urine output, blood pressure, respiratory rate, thoracic imaging as indicated, and weight every few hours.
205
What is the role of C-reactive protein (CRP) in monitoring leptospirosis?
Elevated CRP is common in Leptospira-AKI; its resolution may parallel clinical recovery.
206
What is the rationale behind not using NSAIDs in dogs with leptospirosis?
NSAIDs are nephrotoxic and may worsen GI bleeding and coagulopathies common in leptospirosis.
207
What vaccines are recommended in North America per the 2023 ACVIM update?
Quadrivalent vaccines (Icterohaemorrhagiae, Canicola, Grippotyphosa, Pomona) with two initial doses starting at ≥12 weeks, then annually.
208
How long after doxycycline treatment should dogs be considered non-infectious?
After 48 hours of doxycycline, urine shedding is minimal and zoonotic risk is low.
209
What precautions should be taken for veterinary staff handling suspected leptospirosis cases?
Use gloves, face shield, gown; avoid pressure washing urine; disinfect areas; caution for pregnant staff; minimize movement in hospital.
210
Can vaccinated dogs still get leptospirosis?
Yes, though rare. Leptospirosis has been reported in dogs vaccinated with 4-serovar bacterins. Cross-protection is not always complete.
211
What is the clinical scoring model used to predict outcomes in leptospirosis AKI dogs undergoing dialysis?
Segev’s Model C, which includes variables like urine output, creatinine, bilirubin, albumin, and respiratory involvement.
212
What is leptospiral biofilm and where can it persist?
Leptospira can form biofilms in renal tubules and ocular tissues, allowing chronic carriage even after systemic clearance.
213
What are the public health recommendations from the 2023 consensus?
Vaccinate all dogs, minimize rodent exposure, educate owners, and use protective measures in clinics to prevent zoonotic transmission.
214
What is the goal of the ISCAID 2011 guidelines for urinary tract disease in dogs and cats?
To promote judicious antimicrobial use by providing evidence-based recommendations for diagnosis and treatment of bacterial urinary tract infections (UTIs).
215
What are the clinical categories of UTI defined by Weese et al. (2011)?
Sporadic bacterial cystitis, recurrent UTI, subclinical bacteriuria, pyelonephritis, and catheter-associated UTI.
216
According to Weese et al. (2011), what sample collection method is preferred for diagnosis of bacterial UTI?
Cystocentesis is preferred for culture and sensitivity testing to minimize contamination.
217
When is antimicrobial treatment recommended for subclinical bacteriuria?
Only if the patient is immunocompromised or undergoing urogenital surgery or urinary tract instrumentation.
218
What empirical antibiotics are recommended for sporadic bacterial cystitis in dogs and cats?
Amoxicillin or trimethoprim-sulfonamide, with a short duration (3–5 days) if susceptibility is unknown.
219
What duration of antimicrobial therapy is recommended for sporadic cystitis per ISCAID 2011?
3–5 days with appropriate antimicrobial selection based on updated evidence.
220
What antibiotics should be avoided for empirical treatment of uncomplicated UTIs?
Fluoroquinolones and third-generation cephalosporins, to preserve their use for resistant or serious infections.
221
According to ISCAID 2011, how should recurrent UTIs be addressed?
Investigate and manage underlying causes (e.g., anatomical, functional, systemic), not just treat with repeated antibiotics.
222
What is the preferred diagnostic approach for pyelonephritis in ISCAID 2011?
Blood and urine cultures, with empiric treatment targeting gram-negative organisms, then tailoring to susceptibility.
223
What are the preferred antibiotics for suspected pyelonephritis?
Fluoroquinolones (e.g., enrofloxacin or marbofloxacin), due to good renal tissue penetration and gram-negative activity.
224
What is the 'input sensor' in host-pathogen recognition during a UTI?
Uroepithelial Toll-like receptors (e.g., TLR4) detect pathogen-associated molecular patterns (PAMPs) like LPS.
225
What is the 'controller algorithm' in antimicrobial stewardship?
Clinical decision-making based on culture results, host factors, and infection classification to minimize resistance.
226
What is the 'actuator' in treatment of bacterial cystitis?
The selected antimicrobial drug and its pharmacodynamic effect (e.g., time- or concentration-dependent killing).
227
Why is culture and susceptibility testing strongly encouraged for recurrent or complicated UTI?
To guide appropriate antimicrobial choice and reduce selection for multidrug-resistant bacteria.
228
What defines a complicated UTI according to ISCAID 2011?
UTIs with comorbidities (e.g., CKD, diabetes), urinary tract abnormalities, immunosuppression, or recurrent nature.
229
Why is routine post-treatment urine culture not recommended for uncomplicated UTIs?
Because clinical resolution is sufficient; persistent bacteriuria without signs does not justify further antibiotics.
230
What are the major pathogens of canine and feline UTIs per Weese et al. (2011)?
Escherichia coli, Enterococcus spp., Staphylococcus spp., Proteus, and other Enterobacteriaceae.
231
What is the role of pharmacokinetics in antimicrobial selection for UTI?
Drugs must achieve adequate urinary concentrations; time above MIC or Cmax/MIC ratios are critical for efficacy.
232
How should antimicrobial therapy be adjusted in patients with pyelonephritis?
Initiate with broad-spectrum coverage and tailor based on culture, ensuring adequate renal tissue penetration.
233
How can ISCAID recommendations reduce antimicrobial resistance?
By promoting short-course, targeted therapy and minimizing use of critically important antimicrobials.
234
What supportive diagnostics are recommended for recurrent or complicated UTI workup?
Abdominal ultrasound, contrast imaging, urinalysis, endocrine testing, and advanced culture techniques.
235
How long should pyelonephritis be treated with antimicrobials per ISCAID 2011?
Typically 10–14 days, depending on clinical response and resolution of systemic signs.
236
What does ISCAID recommend regarding catheter-associated UTIs?
Avoid prophylactic antimicrobials; use sterile technique for placement; culture only when clinical signs arise.
237
What are non-antibiotic adjuncts for managing recurrent UTIs discussed in ISCAID 2011?
Cranberry extracts, probiotics, methenamine, and behavioral/environmental modifications (though evidence is limited).
238
What is the clinical significance of bacteriuria without pyuria or signs?
It likely represents subclinical bacteriuria and generally does not require treatment.
239
What was the primary objective of the Whittemore et al. (2011) study?
To evaluate associations between albuminuria, serum C-reactive protein (CRP), survival predictor index (SPI) scores, and survival in critically ill dogs.
240
How was albuminuria assessed in this study?
By measuring the urine albumin-to-creatinine ratio (UACR).
241
According to Whittemore et al. (2011), what UACR value defined albuminuria in critically ill dogs?
UACR >0.03 was considered abnormal.
242
What percentage of critically ill dogs in the study had albuminuria?
64% of dogs had UACR >0.03, indicating a high prevalence of albuminuria in the ICU population.
243
What was the relationship between albuminuria and survival in this study?
Albuminuria was not significantly associated with survival to discharge.
244
According to Whittemore et al. (2011), what was the relationship between UACR and SPI score?
No significant correlation was found between UACR and SPI score.
245
How did CRP concentration correlate with SPI score in this study?
Higher CRP concentrations were significantly associated with higher SPI scores (P = 0.0006), suggesting greater illness severity.
246
What does an elevated SPI score indicate in the context of this study?
Higher SPI scores indicate increased illness severity and decreased likelihood of survival.
247
What is the 'input sensor' that detects inflammation in critically ill dogs?
Hepatic pattern recognition receptors and cytokine signaling pathways (e.g., IL-6) trigger acute-phase responses.
248
What is the 'controller algorithm' for CRP production?
IL-6 stimulates hepatocytes to produce CRP as part of the systemic acute-phase response.
249
What is the 'actuator' for urinary albumin loss in critically ill dogs?
Glomerular barrier disruption (e.g., endothelial glycocalyx injury, podocyte damage) and tubular dysfunction lead to albuminuria.
250
How can albuminuria develop in critical illness without overt renal failure?
Increased vascular permeability, systemic inflammation, and renal tubular injury can cause proteinuria even with normal creatinine.
251
What is the clinical relevance of CRP measurement in the ICU per Whittemore et al. (2011)?
CRP serves as a biomarker of illness severity and systemic inflammation but does not directly predict survival.
252
Why might albuminuria occur independently of CRP elevation?
Albuminuria may reflect local renal or endothelial damage, whereas CRP reflects systemic inflammation.
253
What is a limitation of UACR as a marker in critically ill patients?
UACR may be influenced by urinary concentration, hydration status, and transient glomerular changes.
254
Did CRP or UACR predict survival to discharge in Whittemore et al. (2011)?
Neither UACR nor CRP alone significantly predicted survival to discharge.
255
What physiologic processes contribute to increased urinary albumin in critical illness?
Endothelial injury (e.g., glycocalyx shedding), systemic vasculitis, cytokine-induced permeability, and ischemia-reperfusion injury.
256
What conclusions did Whittemore et al. (2011) draw regarding SPI utility?
SPI was significantly associated with outcome and may be useful in stratifying illness severity in ICU dogs.
257
How does the SPI scoring system work in critical care?
It incorporates multiple clinical and laboratory variables (e.g., lactate, BUN, hematocrit, temperature) to estimate illness severity.
258
What is the clinical implication of this study for ECC?
CRP and SPI may be helpful in monitoring disease progression, but albuminuria alone should not be used to guide prognosis.
259
What was the primary focus of Langston & Gordon (2021)?
To review the physiologic and clinical effects of intravenous (IV) fluid therapy in dogs and cats with acute and chronic kidney failure.
260
What are the main goals of fluid therapy in kidney failure according to Langston & Gordon (2021)?
Restore or maintain perfusion, correct dehydration, manage electrolyte and acid-base imbalances, and promote diuresis in appropriate cases.
261
What is the physiologic rationale for fluid therapy in pre-renal azotemia?
Correcting hypovolemia restores renal perfusion and glomerular filtration rate (GFR), potentially reversing functional azotemia.
262
According to Langston & Gordon (2021), when does fluid therapy fail to reverse azotemia?
In intrinsic (renal) AKI or advanced chronic kidney disease where structural nephron damage limits GFR restoration.
263
What fluid types are most commonly used in kidney patients?
Balanced crystalloids (e.g., Plasmalyte, Normosol-R, LRS) are preferred for most patients; 0.9% NaCl may be used in select cases like hypercalcemia or hyperkalemia.
264
What is the risk of using 0.9% NaCl in large volumes?
May induce hyperchloremic metabolic acidosis, which can worsen renal vasoconstriction and reduce GFR.
265
What is the ‘input sensor’ in renal perfusion monitoring during fluid therapy?
Juxtaglomerular cells detect afferent arteriole stretch and tubular NaCl content via the macula densa.
266
What is the ‘controller algorithm’ regulating fluid response in kidney failure?
The RAAS system (renin release → angiotensin II → aldosterone), along with ADH and natriuretic peptides, governs systemic and renal hemodynamics.
267
What is the 'actuator' during fluid therapy in AKI or CKD?
Administration of IV fluids that increase intravascular volume and renal perfusion, thereby modifying GFR and urine output.
268
According to Langston & Gordon (2021), when is fluid overload most likely in kidney failure patients?
When urine output is reduced (oliguria/anuria) and excessive fluid is administered without adequate monitoring.
269
What clinical signs suggest fluid overload in renal patients?
Peripheral edema, serous effusions (pleural, peritoneal), weight gain, hypertension, and pulmonary crackles.
270
How should fluid therapy be adjusted in oliguric or anuric renal patients?
Use conservative fluid rates and frequent reassessment (e.g., weight, lung sounds, urine output); avoid overload.
271
What is post-obstructive diuresis, and how is it managed?
Polyuria following relief of urinary obstruction; managed with careful replacement of fluid losses to avoid hypovolemia.
272
How does dehydration differ from hypovolemia, and how does it impact treatment?
Dehydration = total body water deficit; hypovolemia = intravascular volume deficit. Rehydration may be slower, while hypovolemia requires rapid correction.
273
What monitoring tools are recommended during fluid therapy in AKI/CKD?
Body weight, urine output, serum electrolytes, PCV/TP, and possibly central venous pressure or point-of-care ultrasound (POCUS).
274
What does Langston & Gordon (2021) recommend regarding the use of synthetic colloids in kidney patients?
Not recommended due to risk of AKI and lack of clear benefit; crystalloids remain first-line.
275
Why is overzealous diuresis discouraged in AKI per Langston & Gordon (2021)?
May lead to volume depletion, worsen renal ischemia, and promote further tubular injury.
276
What is the effect of hyperchloremia on renal perfusion and acid-base balance?
Causes renal vasoconstriction and metabolic acidosis, which may reduce renal blood flow and impair function.
277
How does POCUS aid fluid therapy in kidney failure cases?
Assesses volume status (e.g., IVC collapsibility, lung B-lines) and detects effusions that may indicate overload.
278
What is a conservative maintenance fluid rate in AKI patients with minimal urine output?
Approximately 2–3 mL/kg/h, adjusted based on clinical response and urine production.
279
How does uremia alter fluid distribution and response to therapy?
Uremia can increase capillary permeability and reduce plasma oncotic pressure, favoring third spacing of fluids.
280
What is a critical consideration before administering diuretics in oliguric renal failure?
Confirm volume status and rule out hypovolemia, as diuretics can worsen hypotension and renal hypoperfusion.
281
What acid-base abnormality is most common in kidney failure, and how is it managed?
Metabolic acidosis; managed with fluids, improved perfusion, and sometimes bicarbonate supplementation if pH <7.1.
