9: Frequently Asked Questions (FAQ)

Frequently Asked Questions (FAQ)


FAQ‐01 I usually assume that a patient with a serum creatinine and blood urea nitrogen (BUN) within the reference range does not have kidney disease. Am I safe in this assessment?

  • A: No. A normal BUN or serum creatinine does not necessarily indicate the presence or absence of kidney disease. It is important to remember that BUN and serum creatinine concentrations do not escalate until 50–75% or more of the original nephron mass and glomerular filtration rate (GFR) are reduced (depending on the value for creatinine used for the upper reference limit), so renal disease could still exist. The evaluation of a complete urinalysis (UA) with emphasis on urine specific gravity (USG), proteinuria, and cylindruria will help provide more information as to whether kidney disease exists or not. Renal imaging can also be helpful in determining the presence of renal disease when there are changes in size or shape, echotexture, or corticomedullary junction distinction. Some with primary renal disease do not have abnormalities on renal imaging.

FAQ‐02 I understand that it is difficult in private practice to actually measure GFR using conventional research methods that are highly accurate. Is there something I can do that measure GFR with enough accuracy to be clinically useful?

  • A: YES. You can give an IV injection of iohexol (the same molecule used for contrast urography) followed by the collection of blood samples at timed intervals over a few hours. The rate for the disappearance of iohexol is proportional to the GFR. Only a few laboratories offer the analysis of this molecule unfortunately. The laboratory will calculate the GFR based on the body weight and timing of the blood samples.

FAQ‐03 When is the measurement of GFR something that I need to consider in my patients that I suspect have renal disease?

  • A: The value of GFR is particularly useful in the evaluation of patients that have normal concentrations of BUN, serum creatinine, and symmetric dimethylarginine (SDMA), but yet you still have concerns about the level of renal functions. This is often the situation in those with polyuria/polydipsia (PU/PD) and minimally concentrated urine based on USG. A low GFR in this scenario supports the presence of nonazotemic renal disease that could be associated with the low USG.

FAQ‐04 A five‐year‐old dog with chronic renal disease has a serum phosphorus concentration of 7.1 mg/dL. This result is not cause for concern because it falls within my diagnostic laboratory’s reference range for phosphorus (i.e. 3.5–8.5 mg/dL), right?

  • A: No. Unfortunately, many diagnostic laboratories have reference ranges for serum phosphorus concentration that go up to 8 mg/dL or higher. The reason is because young growing animals with ongoing physiological bone growth have been included in the population used to determine the reference range. A normal mature dog or cat should have a serum phosphorus concentration no greater than 5.5 mg/dL. So, there is reason for concern in this dog especially regarding renal function. The targeted goal for serum phosphorus in chronic kidney disease (CKD) patients is ideally near the middle of the reference range and less than 4.7 mg/dL when possible.

FAQ‐05 Which is better in the evaluation of patients with suspected renal disease, BUN or serum creatinine concentration?

  • A: Neither one is better than the other. Both the BUN and serum creatinine concentrations are insensitive tests for the evaluation of renal function during the early stages of nephron loss. Depending on the upper limits used in the reference range, both the BUN and serum creatinine concentrations begin to increase when 50–75% or more of the nephrons are nonfunctional. BUN, however, is affected by more nonrenal factors than is the serum creatinine concentration, but both have pitfalls in their interpretation. Hence, it is recommended that clinicians evaluate both the BUN and serum creatinine concentrations at the same time.

FAQ‐06 My clinic uses a reference laboratory that does not offer SDMA as part of routine biochemistry measurement. Am I missing out on a better way to look for diseases associated with decreased GFR?

  • A: Yes and No. It is true that SDMA outperforms creatinine for the earlier detection of CKD in both dogs and cats. This means that SDMA will increase above the reference range before creatinine will increase as CKD develops and progresses, especially when the patient has had loss of lean muscle mass (muscle generates creatinine). Greater efficiency in the early diagnosis of CKD can be gained while using creatinine when the upper reference range is lowered to 1.6 for the cat and 1.4 in the dog. Also, trending increases in creatinine within the reference range are useful as are trends for decreasing USG in the earlier detection of CKD.

FAQ‐07 I have a patient with a repeatable increase in SDMA, but the BUN and serum creatinine are in the mid reference range. The USG is 1.030 and higher at times. How do I handle this discordance?

  • A: This type of discordance is common since SDMA escalates before creatinine in many instances of developing CKD. Trending increases in creatinine and or trending decreases in USG provide support that SDMA has been providing accurate information about the presence of renal disease. The measurement of systolic blood pressure and urine protein‐to‐creatinine ratio (UPC) along with renal imaging by ultrasound (ULS) may provide more information about the progression of CKD.

FAQ‐08 Can I trust artificial intelligence/machine learning (AI/ML) algorithms that are designed to predict a future diagnosis of CKD?

  • A: No currently available algorithm is perfect in the prediction of a future diagnosis of CKD using commonly measured analytes (BUN, creatinine, USG, body weight, age, species, protein on dipstrip, urinary pH, and white blood cells [WBC] count on complete blood count [CBC]). These algorithms look for small changes over time in order to make this prediction. A positive prediction for the prediction of CKD over a defined time (one year and two years) would act as an alarm system, warning the attending veterinarian to look more closely at the patient and to measure blood pressure and evaluate proteinuria by UPC or microalbumin (MA). AI/ML for the diagnosis of or prediction of a future diagnosis is in its infancy in veterinary medicine. No studies yet exist to show treatment interventions delay a future CKD diagnosis using AI/ML.

FAQ‐9 On preoperative screening, a seemingly healthy dog has a BUN of 40 mg/dL (30 mg/dL upper reference limit) and a serum creatinine concentration of 1.2 mg/dL (1.6 mg/L upper reference limit). I thought both of these tests usually increased together in the presence of renal disease.

  • A: The most likely cause for such results is that the blood samples were taken within a few (four to eight) hours after a protein‐rich meal, which can result in an increased BUN without a corresponding increase in serum creatinine concentration. A blood sample should be collected after a 12‐hour fast and resubmitted to the laboratory. Dehydration can also result in an increased BUN concentration relative to serum creatinine concentration because urea can be passively reabsorbed into the blood from the renal tubules during decreased tubular flow whereas creatinine cannot. In this instance, the USG is expected to be high due to the renal conservation of water if renal function is normal. Gastrointestinal (GI) hemorrhage is another possible reason why the BUN concentration could be increased disproportionately because the whole blood is a type of high‐protein meal. Alternatively, the increased BUN concentration may accurately reflect poor renal function, while the lower serum creatinine concentration reflects reduced muscle mass in a cachectic animal.

FAQ‐10 I get excited to see the BUN decline when my azotemic patients are eating a renal diet. I tell the owners that this decrease in BUN means that excretory renal function has increased due to the beneficial effects of the renal diet.

  • A: Actually, this decrease in BUN may have nothing to do with any increase in kidney function. When the animal is eating a diet low in protein content but adequate in calories, BUN concentration often decreases because less nitrogenous waste products are generated. In such a situation, BUN concentration is not a good indicator of renal function.

FAQ‐11 I have an older cat with stable CKD over the past two years. Serum creatinine stays at nearly 2.4 mg/dL on all the samples measured every three months. My assessment of this stable serum creatinine concentration is that the CKD is not currently progressive. Am I correct in this thinking?

  • A: A “stable” serum creatinine concentration during CKD is better for the patient than one that is escalating in general. It is important to remember that animals with CKD often lose lean muscle mass that results in less generation of creatinine into the circulation. Loss of lean muscle mass in the absence of renal disease should result in a decreased serum creatinine concentration. Loss of lean muscle mass at a rate proportional to the decrease in GFR in those with renal disease will result in little to no change in serum creatinine. Stable serum creatinine concentration in the presence of ongoing lean muscle mass loss can mask the clinician’s ability to appreciate the progression of renal disease.

FAQ‐12 I have heard that SDMA can be used to replace the evaluation of serum creatinine in patients suspected to have CKD. Should I retire creatinine and instead focus on SDMA?

  • A: No, not entirely. Both creatinine and SDMA are surrogates for GFR. During the development of CKD, SDMA often increases quite a bit earlier, before increases in serum creatinine are recognized. Much of this early increase in SDMA likely occurs since SDMA is not influenced by body weight/condition whereas creatinine is. Creatinine is generated from within muscles, so with loss of lean muscle mass that often accompanies CKD, there is less creatinine entering the circulation and a lower serum creatinine will be measured. The usefulness for the evaluation of serum creatinine is improved when a lower upper reference range is used, instead of the larger population‐based reference range (e.g. <1.6 mg/dL for cats and <1.4 for dogs). It is always better to measure and assess multiple surrogates of GFR at the same time to limit the chances for errors in interpretation. Discordance in results for surrogates of GFR happens at times.

FAQ‐13 As I understand it, SDMA increases only in primary renal disease and not in prerenal or postrenal conditions. Is this true?

  • A: No. SDMA, like creatinine and BUN, will be influenced by anything that alters GFR. SDMA will increase during prerenal, postrenal, and primary renal conditions that decrease GFR. SDMA will decrease during hyperthyroidism as GFR increases.

FAQ‐14 I usually bias my evaluation of serum biochemistry results in my CKD patients to BUN, creatinine, and SDMA. Are there other analytes to which I should also give attention?

  • A: YES. Circulating phosphorus is a very important molecule to follow for its potentially detrimental effects on soft tissue calcification and effects that can increase PTH and FGF‐23. Calcium is also important especially during interactions with increased phosphorus that increase the Ca × P product. Potassium and TCO2 (close approximator of HCO3) also deserve your attention.

    Close attention to circulating calcium, phosphorus, and Ca × P product is a good idea when following CKD patients that are treated with calcitriol.

FAQ‐15 How important is it to monitor circulating calcium concentrations in dogs or cats with CKD?

  • A: Most patients with CKD have normocalcemia, but some will be observed with either hypocalcemia or hypercalcemia based on total serum calcium measurements. Unfortunately, discordance between total serum calcium and ionized calcium occurs frequently, especially during states of azotemic CKD. Many CKD dogs with high total serum calcium have normal ionized calcium concentrations likely due to increased concentrations of complexes that bind calcium during CKD; this phenomenon is far less common in cats. It is important to know if the high total calcium is also associated with high ionized calcium, since only increases in ionized calcium are toxic to the animal.

    Trending increases in both total serum calcium and ionized calcium that are still within the reference range have recently been associated with the progression of CKD in the cat. Some cats with early stages of CKD develop hypercalcemia while eating a renal diet that is too restricted in phosphorus; the high Ca:P ratio appears to facilitate calcium absorption across the intestine.

FAQ‐16 How important is it to monitor serum potassium levels in patients with CKD or acute kidney injury (AKI)?

  • A: Hypokalemia occurs in some patients with CKD, especially in cats. Hypokalemia can develop secondary to CKD, but it appears that hypokalemia can also create CKD. Hypokalemia can exert deleterious effects on excretory renal function and can be associated with less ability to concentrate urine. Hypokalemia results in functional changes that decrease kidney function initially but structural changes can occur later. Hyperkalemia is of concern in some patients with AKI, especially those that have oligo‐anuria.

FAQ‐17 Should I recommend renal biopsy more often in my persistently azotemic patients?

  • A: Renal biopsy should not be approached lightly because complications are possible (hemorrhage and renal damage). The kidney should be biopsied only if the results are likely to change how the patient is treated. ULS‐guided biopsy of small kidneys in CKD should not be undertaken due to the risk of hemorrhage and the oftentimes unrewarding pathology findings due to extensive fibrosis. Examples of situations in which the information obtained from renal biopsy may change your approach to management include: differentiating acute from chronic renal failure when this is not apparent after thorough clinical evaluation, establishing a prognosis in AKI when the clinical course has been protracted, and differentiating glomerulonephritis (GN) from glomerular amyloidosis in those with CKD. Distinguishing between AKI caused by nephrosis or that caused by nephritis can be helpful, especially for patients suspected to have leptospirosis. It is less rewarding to perform renal biopsy in patients with stage 3 or 4 CKD, as primary renal lesions may not be apparent due to extensive tubular atrophy, glomerular sclerosis, and interstitial fibrosis. Renal biopsy earlier in the course of CKD may be especially helpful in patients with renal proteinuria if the biopsy can undergo full evaluation using light microscopy, electron microscopy, and immunofluorescent antibody (IFA). Treatment protocols are emerging in veterinary medicine that are designed for a specific histopathological diagnosis in those with GN. Systemic blood pressure should be normalized prior to renal biopsy, a procedure that should be performed by a highly skilled operator and experienced hospital that is able to deal with any complications.

FAQ‐18 Why is the measurement of serum albumin and cholesterol concentrations important to monitor in patients with CKD?

  • A: Low serum albumin and high cholesterol during CKD can be associated with protein losing nephropathy in some dogs. The measurement of UPC is indicated now, if it has not already been determined, to assess the magnitude of proteinuria and its likely contribution to the hypoalbuminemia. High cholesterol concentration in cats with CKD is common and does not raise concern for PLN as it does in dogs. Animals consuming renal diets can develop hypoalbuminemia and hypercholesterolemia as a result of too little dietary protein.

FAQ‐19 How can I best know if abdominal effusion following trauma is urine or not?

  • A: Following abdominocentesis, the abdominal fluid creatinine concentration to serum creatinine concentration ratio is usually >2:1 if the fluid is urine due to delayed uptake of creatinine in this fluid across the peritoneum. Urea nitrogen ratios are not as useful since urea is more readily reabsorbed from the peritoneal cavity. If the abdominal fluid‐creatinine‐concentration‐to‐serum‐creatinine‐concentration ratio is equivocal (i.e. ≤2:1), calculate the abdominal fluid potassium concentration to serum potassium concentration ratio. Patients with uroperitoneum will have a ratio of >1.4 (dogs) or >1.9 (cats). Determining the site of the urine leakage is the next step using some form of contrast urography. Uroabdomen occurs most often from ruptures in the bladder. The retrieval of urine following urethral catheterization does not exclude the possibility for a ruptured bladder.

FAQ‐20 Last week, I euthanized a 17‐year‐old cat that was presented for the evaluation of anorexia and vomiting. Serum creatinine concentration was >20.0 mg/dL. The kidneys were slightly small on palpation and the cat was approximately 10% dehydrated based on skin turgor assessment. The cat was euthanized with a presumed diagnosis of azotemic CKD. On necropsy, there was a considerable amount of abdominal fluid and a small hole in the bladder surrounded by a large bruise. Could all of these findings be associated with urine leakage from the bladder into the abdomen?

  • A: Yes. The magnitude of azotemia does not differentiate among prerenal, primary renal, or postrenal causes. Many older cats have CKD and some degree of azotemia, but older cats also may experience bladder rupture following trauma, as was the case in this particular cat. The kidneys were normal at necropsy. It is always a good idea in any case with azotemia to ask the question, “Could it be prerenal, primary renal, or postrenal in origin?”

FAQ‐21 I have heard that it is important to evaluate thyroid function in all cats with suspected or confirmed CKD. The term “masking” has been mentioned in this situation, but I am not sure just what that means.

  • A: Excess thyroid hormones in the body increase both renal blood flow and GFR such that excretory renal function is enhanced. This means that the surrogates of GFR (creatinine and SDMA) will be lower than during the euthyroid state. Restoration of T4 to the reference range following treatment (I‐131, methimazole, and surgery) will decrease GFR and increase creatinine and SDMA concentrations. The increase in creatinine post‐treatment is often mild but can be of high magnitude in some cats. For example, in a cat with a high T4 and a creatinine of 1.8 mg/dL, the post‐treatment creatinine increased to 2.5 mg/dL at a time that T4 was in the reference range. The initial 1.8 mg/dL creatinine was this low because of the high thyroid status that had increased GFR, thus masking the degree of excretory renal failure that only became obvious after the T4 was reduced.

FAQ‐22 I have a 14‐year‐old spayed female domestic shorthair cat presented for PU and PD along with severe weight loss and fairly normal appetite. A thyroid nodule is consistently palpable on the left side of the trachea. The kidneys are approximately 3.0–3.5 cm in length and feel smooth on palpation. USG is 1.019, serum creatinine is 2.0 mg/dL, and BUN is 38 mg/dL. The T4 is about 2× increased beyond the upper reference range. What can I expect following radioiodine treatment for the hyperthyroidism?

  • A: The creatinine is mildly increased in the face of hyperthyroidism and urine that is minimally concentrated. Hyperthyroidism increases GFR, which decreases the creatinine concentration. So, we should expect to see some increase in serum creatinine when euthyroidism has been restored. The increase in serum creatinine following the restoration of euthyroidism is modest in most cats.

FAQ‐23 I am treating a hyperthyroid cat with oral methimazole. The T4 concentration decreased to within the mid reference range at the same time that the serum creatinine increased from 1.7 to 2.4 mg/dL. Should I decrease the dose of the methimazole to keep the creatinine at a lower value?

  • A: No. It is unlikely that the cat knows that its current creatinine has escalated by 0.7 mg/dL. Lowering the dose of methimazole will allow the T4 to increase and that will increase GFR and lower the creatinine. The ongoing hyperthyroidism, however, will result in glomerular hypertension and progressive renal injury. So, it is better to become euthyroid and to tolerate the “exposed” increase in serum creatinine in general.


FAQ‐24 Is it best to perform the complete UA in‐house or to send it out to a reference laboratory?

  • A: There is no set answer for all practice situations. If you currently perform few complete urinalyses in‐house, sending urine to a reference laboratory offers a way to increase diagnostic information for your patients without consuming in‐house personnel time. The training of technicians to perform in‐house UA varies widely among practices. Sending urine to a reference laboratory makes sense if your technicians do not have the skill set and training needed to accurately and consistently perform urine microscopy, which is the biggest stumbling block to performing in‐house UA.

    Some practices have highly skilled technicians that efficiently, consistently, and accurately perform the complete UA. The workflow to make this happen is not linear and takes from about 18–22 minutes to complete. Performing in‐house urinalyses allows more money to be generated for the practice compared to sending out the urine to a reference laboratory.

    The sicker an animal is, the more important it is to perform the complete UA in‐house so that abnormalities of importance are detected and reported. Fragile elements like cellular casts are unlikely to be detected in samples sent to reference laboratories. Lower numbers of cells and casts along with more crystals are likely to be reported from samples that undergo storage and shipping to a reference laboratory. There is less urgency to perform in‐house UA for apparently normal animals (pre‐op, wellness, and geriatric).

    Performing the UA in‐house gives the attending DVM the chance to have a conversation about the results while the owner is still at the practice. Sending the UA to a reference laboratory usually involves a 5–24‐hour delay in obtaining the results, depending on when the sample is picked up and processed by the laboratory.

FAQ‐25 I keep hearing about “automated” UA. Is this just a fad, or should I consider this for use in my practice? Is it better than the traditional manual methods?

  • A: Automated UA is not just a fad and is likely to become the standard for in‐house UA in the near future. “Automated” refers to both the measurement of chemistry by urinary dipstrip and urine microscopy. USG still needs to be done manually in‐house.

    Urine chemistry is more accurate and more consistent when determined with a reader that removes the subjectivity of a human deciding on the degree of color reaction that will be reported.

    Automated urine microscopy is very good at identifying red blood cells (RBC), WBC, epithelial cells, hyaline casts, and bacteria, but not yet as good as that determined by human experts. The algorithms used to identify urinary elements continue to improve over time and so the accuracy of reporting will continue to improve during automated microscopy. Clumping of WBC or epithelial cells is not yet part of automated reporting, and characterization of casts beyond nonhyaline is problematic.

    Automated microscopy generates a report that enumerates urinary elements within three minutes. Results of the complete UA are generated within five to six minutes accounting for the time to measure USG by refractometry, automated urine chemistry, and automated microscopy. The technician still needs to take about another minute to make sure that the microscopy results on the report match up with that seen on the digital pictures taken by the machine. Workflow efficiency is improved using automated methods compared to the manual method that consumes from 18 to 22 minutes of nonlinear personnel time. Clients appreciate receiving the UA reports generated, while they are still on site and more readily understand their costs for this testing.

FAQ‐26 How can I justify the expense of a machine to perform automated urine microscopy? The equipment is rather expensive.

  • A: Yes. The one‐time expense to purchase the urine microscopy analyzer is high. If you are currently submitting few UA for complete analysis, then the use of the automated analyzer will allow the practice to ramp up to do a lot more UA without consuming a lot more personnel time while generating additional income that will pay for the machine. If you are sending out most of your UA currently, switching over to the automated analyzer will allow increased accuracy of results due to decreased generation of artifacts (e.g. crystal growth and bacterial growth) during cooling and transport and increased ability to identify elements in fresh urine that have not undergone degeneration or loss during transport to a laboratory. Fresh warm urine always wins.

    If you are routinely doing UA by manual methods – you can continue to do so, or you can consider giving the automated methods a try to see how your practice workflow might improve that can allow you to perform even more complete UA.

FAQ‐27 I am skeptical that a machine can be as accurate during urine microscopy as that recorded by my experienced technicians. I have compared the results from the automated to the manual method and they are not always the same. Is it good enough?

  • A: You are correct that results between automated and manual methods of urine microscopy are not identical. Nor should they be. Differences in the methods as to how the urine is handled can account for this – volume, centrifugation force, and level of observer skill. Though there will be differences in the enumeration of elements, that difference is likely to be small. Differences in the identification of elements will also occur; automated methods are not as good in the identification of more uncommon elements.

    YES, it is good enough for the identification of routine elements like RBC and WBC. Pretty good for the identification of squamous and nonsquamous epithelial cells. Really good at the identification of rod bacteria. Cocci identified by the machine should be confirmed on the visual analysis of digital images. Good for the identification of hyaline casts, but not able yet to determine other than nonhyaline casts – the technician must examine the digital images to determine if the nonhyaline casts are granular, waxy, or cellular. Digital pictures should also be examined to ensure that crystals other than struvite or calcium oxalate are not present.

    In some instances, results from automated microscopy will be more accurate than elements reported by manual microscopy, depending on the level of expertise of the technician.

FAQ‐28 I am not comfortable with the change in the reporting of results in urinary sediment from per high‐power field (HPF) or per low‐power field (LPF) to per μL. Why is it now considered better to report results as per μL rather than the time‐honored method of per HPF or per LPF?

  • A: This is the future to which we should be moving. Enumeration per μ L is more accurate than when reporting as per HPF or per LPF for several technical reasons related to the set up for urine microscopy. This type of counting is already conventional for hematology and fluid cytology results. The per HPF or per LPF method is an approximation of a volume that is examined, but this varies considerably by the dynamics of the microscope optics as to what is a “field,” the thickness of the drop examined, and the size of the coverslip.


FAQ‐29 I have been told that it is generally not worth examining urine collected by voiding and that only samples collected by cystocentesis should be submitted. Is that true?

  • A: No, not entirely. It is true that samples collected by cystocentesis avoid lower urinary and genital contamination with bacteria, cells, and protein, which lessens confusion as to what is pathological or not. Samples collected by cystocentesis often have extra RBC from the trauma of this method, regardless of operator skill in performing the cystocentesis. There is no easy way to know with certainty that RBC in samples collected by cystocentesis are there from underlying disease or trauma during bladder entry and manipulation of the cystocentesis needle.

    Voided urine, preferably mid‐stream, still generates value in the analysis of USG, urine chemistry, and urine microscopy showing the presence of abnormal elements. Also, actually going out with the client to watch the dog urinate can provide valuable information as to the nature and character of the act of urination. If the urinary sediment is silent – there is no need to collect another sample by cystocentesis. If the urine sediment is active, it might be a good idea to confirm these results using a sample collected by cystocentesis. Increased RBC shown on a sample collected by cystocentesis but absent on a voided urine sample suggests that trauma from the cystocentesis accounts for the RBC.

    End‐urination voided urine samples may prove especially fruitful in the identification of malignant epithelial cells from those with transitional cell carcinoma (TCC) of the bladder. Also, end‐urination samples can yield more crystalline material that has settled out in the bladder at times. Initial‐voided urine samples reflect more of what is going on in the urethra and genital tracts.

FAQ‐30 Is it OK to culture urine collected during voiding for bacteria?

  • A: Culture of urine is best interpreted on samples collected by cystocentesis since bacterial contamination of the lower urogenital tract is avoided. Culture of voided urine that shows no growth provides useful results. Positive bacterial growth on voided samples is often problematic, as we often do not know with certainty that the isolated organisms are pathological or if they grew from lower urogenital (UG) contamination. Older literature indicated that this was particularly a problem in female dogs that could have abundant growth of organisms on culture of voided samples but not from the same dog’s urine collected by cystocentesis. More recent thinking is that culture of voided urine can accurately reflect the presence of a bacterial urinary tract infection (UTI) if a single organism grows in large quantity (>100 000 cfu/mL in female dogs and >10 000 cfu/mL in male dogs and in cats). It is always best to culture urine collected by cystocentesis if there is uncertainty about culture results generated from voided urine or from catheterized urine samples.

FAQ‐31 I was taught to never perform cystocentesis in a dog or cat with urethral obstruction (UO) and a large bladder – largely due to fears of rupturing the bladder and/or creating uroabdomen. I have heard from others that cystocentesis can safely be performed in this setting. Is this true?

  • A: Yes, in general when performed by an experienced operator. The procedure should be that of decompressive cystocentesis and not just removal of a small volume to submit for UA. Nearly complete evacuation of urine from the bladder allows time for the cystocentesis tract to seal in the absence of high pressure. Collection of urine by cystocentesis allows the analysis of a urine sample before urethral and bladder manipulation have taken place during attempts to relieve the UO. Contamination or dilution of the urine sample is avoided when cystocentesis is performed before alleviation of the UO. It is likely that decompressive cystocentesis facilitates relief of the UO during hydropulsion needed to flush obstructing material (plugs and stones) from the urethra into the bladder.

    In cats with UO, some abdominal effusion often exists prior to any urethral manipulation, instrumentation, or cystocentesis. Some abdominal effusion can become apparent post cystocentesis, but this volume is small and is resorbed soon after UO is relieved (indwelling urethral catheter). Postcystocentesis leakage of bladder contents is less likely to occur when the bladder has undergone removal of as much urine as is feasible.

FAQ‐32 I have heard that it is nearly meaningless to evaluate UA results from dogs or cats in which the urine was collected by catheter. Is this true?

  • A: No, depending on the operator’s skill in atraumatic passage and placement of the urethral catheter. USG and most urinary dipstrip chemistry results will be clinically useful. Urinary sediment could potentially be active as an artifact due to the addition of RBC and epithelial cells as a consequence of trauma from this technique of urine collection. Bacteria can be added to the urine sample during the passage of the urinary catheter as another artifact. Bacterial culture from urine samples collected by urethral catheterization can yield large positive growth at times from contamination, especially in female dogs.

FAQ‐33 I stopped performing cystocentesis in cats due to very scary episode I had in one cat that collapsed during the procedure. Is this a common adverse effect?

  • A: Collapse during cystocentesis rarely happens in some cats. And yes, it can be frightening to observe. This collapse is probably related to a vagal–vagal response during the procedure. Recovery following the collapse is usually rapid if there are no underlying cardiovascular problems that promoted the collapse. This has been observed in some cats that were highly agitated before the procedure. Mild sedation prior to cystocentesis is recommended in these instances. We have observed acute collapse in some male cats with UO in which removal of urine was very rapid during therapeutic decompressive cystocentesis.

FAQ‐34 How can the number of crystals vary so drastically in samples collected by cystocentesis compared to voided urine?

  • A: In some instances, a high crystal burden can settle out into dependent regions of the bladder. Consequently, the cystocentesis needle can be aimed above the dependent regions of crystal accumulation and the recorded number of crystals will be low. We recommend agitating the bladder to resuspend crystals immediately before the cystocentesis in order to retrieve a more representative sample. Alternatively, an end‐urination urine sample will retrieve the settled‐out crystals. Similarly, more crystals can be retrieved via urethral catheter as bladder urine is fully emptied.

FAQ‐35 I have noticed substantial discordance in urine microscopy results when the same urine sample was examined a second time shortly after the first examination. How is this possible?

  • A: This is not an uncommon phenomenon. It likely happens when one of the two urine samples was not well‐mixed immediately before preparation of the urine sample for microscopy. Elements in urine can settle by gravity very quickly, so it is easy to submit a nonrepresentative portion of the urine above that which has settled. This is an example of a preanalytical error. It is essential to ALWAYS well‐mix the urine sample before analysis.


FAQ‐36 If the urine is a medium to dark yellow color, I often assume that the urine is well concentrated. In these instances, in an animal that appears otherwise healthy, I do not measure the USG. Is this practice OK?

  • A: No. It is true that the amount of yellow color to the urine varies somewhat by how concentrated that urine sample is. Urine with very little color is often dilute and urine with deep yellow color is often concentrated. There are many instances of discordance between an estimated USG based on urine color and USG measured on a refractometer. It is often important to know the actual USG rather than some guesstimate. How dilute or how concentrate the sample is good to know. Urochromes largely contribute to the urine color, but their presence varies by each individual.

FAQ‐37 I just examined a urine sample that appeared dark brown to black in color. The dog is sick but has no urinary signs. After centrifugation, the supernatant is the same color and there is no obvious sediment. Urine microscopy reveals very few of any type of elements. What is causing the dark coloration to this urine?

  • A: Since the color persisted after centrifugation and the urinary sediment was inactive, the color has to be from something dissolved in the urine rather from formed elements that would have gravitated into sediment. Though hemoglobinuria and myoglobinuria can both create pink urine, both can also appear black following some degree of oxidation in the urine. If the CBC shows normal RBC counts and appearance, hemolysis is unlikely to be generating enough hemoglobin to enter the urine. Myoglobinuria is a more likely cause in these instances. Increased serum CK is supportive for rhabdomyolysis that could allow enough myoglobin to enter and discolor the urine. Though not commonly performed, there are tests to definitively differentiate between myoglobin and hemoglobin in the urine.

FAQ‐38 A three‐month‐old pure‐bred dog is presented for evaluation of PU, PD, dilute urine (USG 1.012), and moderate azotemia (serum creatinine concentration 3.7 mg/dL). Proteinuria (2+) is found on urine dipstrip evaluation. The health status of the other littermates cannot be determined. What is the chance that this dog has a familial nephropathy?

  • A: It is very possible that the dog indeed has a familial nephropathy. It is also possible, however, that renal disease was acquired in utero or soon after birth as a result of nongenetic factors. Information from diagnostic imaging and UPC can provide support for this diagnosis, but renal histopathology using light microscopy, electron microscopy, and evaluation with IFA will be needed to make a definitive diagnosis.

FAQ‐39 An 11‐year‐old castrated male German Shepherd Dog has been definitively diagnosed with hyperadrenocorticism (HAC) and treated with trilostane, leading to a hypoadrenal crisis in the past. Pre‐ and post‐adrenocorticotropic hormone cortisol concentrations are currently within the normal range. Persistent and severe PU and PD developed in the last month. Serum biochemistry results, including BUN and serum creatinine concentrations, are normal. Urinalysis was normal, with the exception of a USG of 1.010. The USG was still 1.010 after gradual water restriction to 30 mL/lb/day. Results of abdominal radiographs and abdominal ULS imaging are normal. The dog was given 0.2 mg DDAVP orally twice a day which resulted in a USG of 1.040. The USG returned to 1.010 shortly after the DDAVP tablets were discontinued. Does this dog have central diabetes insipidus (CDI)?

  • A: Apparently so. The dramatic response to the DDAVP followed by a rapid return to much more dilute urine in the absence of DDAVP supplementation supports a diagnosis of CDI. The possibility of a mass lesion in the region of the pituitary gland and the hypothalamus should be considered.

FAQ‐40 Is a USG in the hyposthenuric range (1.001–1.006) required to diagnose CDI?

  • A: No. Animals with complete CDI typically have hyposthenuria (USG 1.001–1.006), but some dogs with complete CDI can concentrate above this range despite complete absence of ADH if they are dehydrated (but usually not above USG 1.017). An alternate explanation is that the dog has partial CDI. Brain imaging (magnetic resonance imaging or computed tomography [CT]) can be performed to evaluate the hypothalamus and pituitary gland for diseases that could interrupt production or secretion of ADH.

FAQ‐41 I have encountered a USG from a dog that was 1.000. I thought that might be an analytical error, so I repeated the measurement using the same urine sample and the same refractometer as before, and it was again 1.000. I have never seen a USG this low. The dog has mild PU, but I was not expecting to find a USG this low. Is this a “real” USG? The urine was collected free‐catch by the owner.

  • A: Probably not. Something else is happening here. If the 1.000 USG were real, one would expect the dog to have severe PU/PD and that is not the case. It is possible that the sample is not really urine, or that it has been diluted accidentally with water. Repeat the USG on another sample to see if the USG is still the same or not. It most likely is NOT.

FAQ‐42 The owners of a 13‐week‐old male Labrador retriever are having difficulty housebreaking the puppy. The dog seems to drink constantly and urinates while walking around the house. Urinalysis was normal except for a USG of 1.003. Could this dog have CDI?

  • A: CDI is possible, but psychogenic PD (PPD) is far more common in puppies. Some puppies drink water in excess of their physiological need. They usually outgrow this tendency by the time they are four to six months old. If necessary, PPD can quickly be differentiated from CDI during water deprivation testing (WDT). This dog’s USG was >1.040 after approximately six hours of water deprivation, confirming normal urinary concentrating ability. If the dog had CDI, its USG would have remained low and would not have increased to more than 1.017 when dehydrated. Sometimes gradual WDT is needed to counteract MWO from severe PU/PD before urinary concentration capacity is fully restored.

FAQ‐43 We anesthetized an 11‐year‐old spayed female mixed breed dog for dental extractions. Her history indicated no problems, and she was normal on physical examination before the dental procedure. CBC and serum biochemistry results also were normal before the procedure, but no UA was performed. Anesthesia and the dental procedure lasted approximately one hour, and she received some intravenous fluids during this time. The nonsteroidal anti‐inflammatory drug (NSAID) carprofen and the antibiotic enrofloxacin were prescribed for one week after the procedure. A few days after release from the hospital, the owners reported that the dog was drinking quite a bit of water and urinating large volumes. Urinalysis at this time was normal except for a USG of 1.010 and trace proteinuria, and urine culture showed no growth. Serum biochemistry results at this time were still normal. A low dose dexamethasone test to evaluate for HAC was normal. What can I tell the owner?

  • A: More information is needed. It would have been helpful to have UA results (especially USG) before anesthesia. In dogs with underlying renal disease, UA results are likely to be abnormal long before changes in serum biochemistry become apparent. Some dogs with chronic nonazotemic renal disease decompensate after anesthesia. NSAID administration could have transiently affected urine concentration. Some dogs develop renal medullary washout (which can persist for several weeks) after anesthesia and IV fluid administration. The determination of iohexol clearance would identify if GFR is decreased despite normal BUN and serum creatinine concentrations. If GFR is decreased, the dog likely has nonazotemic chronic renal disease that has been pushed over the edge somewhat. If GFR is normal, gradual water deprivation could be performed to determine if renal medullary washout has occurred. This procedure also will help to correct renal medullary washout if it is present.

FAQ‐44 Is there any benefit to perform WDT in dogs or cats suspected to have underlying CKD?

  • A: WDT should not be performed in an animal is known to have underlying renal disease. Dehydration that arises during this testing can pose a risk to develop AKI in the remnant nephrons if enough renal ischemia develops. The risk of ischemic renal damage during WDT is far greater in patients with diseased kidneys than in those with normal kidneys, especially if they are overtly azotemic. The reason(s) for the inability to adequately concentrate urine are readily explained by the primary renal disease and no extra benefit is gained by WDT.

    In some instances, it is not clear in the nonazotemic patient if the cause of impaired ability to elaborate concentrated urine (low USG) is created by chronic renal disease or some other underlying disease associated with PU/PD. In such instances, careful monitoring during water deprivation is crucial to ensure that those with underlying kidney disease are not further injured by the WDT. The use of gradual water deprivation at home can be useful in these instances.

    Desmopressin testing and/or GFR measured by iohexol clearance are often better choices to further evaluate renal function and ability to concentrate urine in fragile patients.

FAQ‐45 In what diseases is WDT most likely to help me determine the definitive diagnosis?

  • A: WDT is used primarily as a tool to distinguish among CDI, nephrogenic diabetes insipidus (NDI), and PPD. WDT usually substantially increases in those with PPD and fails to increase the USG in those with CDI and NDI. After failed WDT, a large increase in USG following the administration of desmopressin supports the diagnosis of CDI. Failure to increase the USG after administration of desmopressin supports the diagnosis of NDI (including those with MWO).

FAQ‐46 Is it better to perform a 12‐hour or a 24‐hour abrupt water deprivation test?

  • A: NEITHER. There should be no such thing as a predetermined 12‐hour or 24‐hour period for the abrupt WDT. WDT should be tailored to each patient individually; following USG or Uosm sequentially hourly until a steady state has been reached, or when body weight loss approaches 5%. In some instances, WDT will be over in a few hours if maximal urine concentration is achieved (as in PPD). WDT will also be terminated within a few hours if obligatory PU continues (CDI, NDI) and dehydration develops. It is essential to closely monitor all patients during WDT to ensure that they are not injured by dehydration during this testing (e.g. AKI). Some have referred to WDT as “barbaric,” which it can be if the patient is not carefully monitored. Desmopressin testing usually is the next diagnostic step for those that fail WDT. Alternatively, desmopressin testing could be used instead of WDT as it is easier and safer for fragile patients, though a positive response can happen in those with CDI or those with MWO from any other cause.


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Apr 18, 2023 | Posted by in SMALL ANIMAL | Comments Off on 9: Frequently Asked Questions (FAQ)

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