Review of Azotemia in Foals

MEDICINE II

Harold C. Schott II, DVM, PhD, Diplomate ACVIM

1. Introduction kidneys increase in size through the first 1 to 2 years Azotemia in neonatal foals (Յ7 days of age) may be of life. Foals are born with about 10 million glom- an indicator of pre-renal failure, acute kidney injury eruli in each kidney, and these enlarge in size as the 2 (AKI), obstructive disease, congenital renal disor- kidneys grow. Of interest, low birth weight and ders, or disruption of the collecting system leading to premature infants may be born with fewer uroperitoneum. Because clinical signs of renal fail- nephrons, and there is mounting evidence that this ure may be similar to those with septicemia or as- reduced renal endowment may increase the risk of phyxia (weakness, recumbency, or poor nursing developing hypertension and chronic kidney disease vigor), performing a serum biochemical analysis in (CKD) in later life.3 compromised neonates is an essential part of the Normal term colts typically first urinate between minimum database to detect azotemia. Spurious 5 and 6 hours of age, whereas fillies initially urinate hypercreatininemia may also be a transient finding later, at 10 to 11 hours of age.4 Initial urine may be in asphyxiated foals or foals delivered from mares dilute or concentrated (specific gravity up to 1.040), with placentitis.1 Neonates with spurious hyper- but hyposthenuria develops by 24 hours of age in all creatininemia have normal serum electrolyte con- foals that are nursing well. Urine pH is nearly centrations, supporting normal renal function, and neutral, and significant proteinuria (2 to 3ϩ on re- creatinine concentration, which may exceed 20 mg/ agent strips) is commonly observed from 24 to 48 dL, typically drops by 50% or more over the first 1 to hours of age in foals that received good passive 2 days of life, as long as foals are well hydrated and transfer of colostral antibodies.5 Serum urea nitro- nursing well (Fig. 1). In older foals, azotemia and gen (BUN) and creatinine (Cr) concentrations are renal failure are almost always a consequence of variable during the initial 24 hours of life, with another primary disease process, although limited values in the range of 15 to 30 mg/dL (ϳ5–10 renal function with congenital anomalies may delay mmol/L) and 2 to 4 mg/dL (ϳ175–350 ␮mol/L), re- onset of renal failure until foals are several years spectively. BUN generally drops below the lower old. limit of the adult reference range by 24 hours of age, whereas Cr may not drop below 2 mg/dL until 48 2. Neonatal Renal Development and Physiology hours of age. By 1 to 2 weeks of age, BUN is typi- Nephrogenesis, in terms of nephron numbers, is es- cally below 10 mg/dL (ϳ3.5 mmol/L) and Cr may fall sentially complete at birth, and, as foals grow, the below 1.0 mg/dL (ϳ90 ␮mol/L). These low values

NOTES

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25 Renal tubular function remains essentially normal with pre-renal failure. Thus, serum electrolyte concentrations are typically normal, and urine so- a 20 dium concentration is Ͻ20 mEq/L. Depending on hydration status, urine specific gravity may be vari- 15 able, but the classic finding that supports pre-renal azotemia is a specific gravity Ն1.025 and a urine a,b osmolality (Uosm) exceeding 500 mOsm/kg. 10 4. Intrinsic Renal Failure Intrinsic renal disease and acute renal failure (ARF) 5 b,c can develop as a consequence of hypoxic-ischemic

serum creatinine (mg/dl) c injury associated with birth asphyxia, septicemia, 0 or leptospirosis or treatment with nephrotoxic admission day 2day 3day 4 medications (aminoglycoside antibiotics and NSAIDs).11,13–17 It is often difficult to separate the Fig. 1. Decline in serum creatinine concentration in 28 equine effects of these factors because many compromised neonates that were admitted at 48 hours or less of age with a Ͼ foals are routinely treated with nephrotoxic medica- serum concentration 5 mg/dL attributed to spurious hypercrea- tions. Over the past decade, there has been a shift tininemia. Note the Ͼ50% decline in serum creatinine concentration within the initial 24 hours of therapy (from admission to day away from routine use of penicillin and an amino- 2). glycoside for broad-spectrum antimicrobial therapy of neonatal foals (largely replaced by ceftiofur), and this change has probably decreased the incidence of aminoglycoside nephrotoxicity in foals. Further, the shift away from multiple daily doses to once- can be attributed to the large volume of fluid intake daily dosing regimens for aminoglycoside antibiotics as milk (5-fold greater fluid intake as compared with has been well documented to decrease the risk of adult horses on a mL/kg basis) and associated diure- nephrotoxicity in infants.18 Unfortunately, during sis that may persist for the first 3 to 4 months of life, the same time period there has been increased use of as long as foals continue nursing their dams.6 oxytetracycline in foals with contracted tendons, Renal function of neonatal foals, as assessed by and tetracycline-associated ARF may go undetected glomerular filtration rate (GFR), is similar to that of in compromised neonates unless a serum chemistry adult horses.7,8 Further, the kidneys of foals are profile is submitted as part of case management. capable of excreting a sodium load provided by fluid The incidence of ARF in foals in neonatal intensive administration,9 and fractional electrolyte clearance care units is not well documented, but human neo- values are similar to those of adult horses, support- natal intensive care units have reported incidences ing that renal tubular function in foals is similar to ranging from 6% to 24%, with cardiac surgery and that of adult horses.5 severe asphyxia being recognized risk factors. Of interest, ARF was nonoliguric, oliguric, and anuric 3. Pre–Renal Failure in 60%, 25%, and 15% of patients, respectively.11 Renal hypoperfusion leading to pre-renal azotemia Consequently, adequate urine production cannot be is common in compromised neonates. Several com- used to exclude AKI and ARF in compromised pensatory mechanisms accompany decreased renal equine neonates. perfusion to maintain renal blood flow and GFR over Although there are no specific values for BUN and a range of perfusion pressures (autoregulation). Cr that separate pre-renal failure from intrinsic re- These include a decrease in afferent arteriole tone nal failure, azotemia is generally greater with in- and intrarenal production of vasodilatory prosta- trinsic renal failure. Further, there is not a sudden noids (PGE2 and PGI2) to maintain blood flow, par- transition from pre-renal failure to intrinsic renal ticularly in the medulla.10 Renal hypoperfusion failure; rather, these are overlapping conditions. increases the risk of nonsteroidal anti-inflammatory To emphasize the point that some intrinsic renal drugs (NSAID) associated AKI; for example, nearly damage probably occurs with simple renal hypoper- 40% of premature infants that receive indomethacin fusion, the term acute kidney injury, characterized to speed closure of the ductus arteriosus develop by a 50% increase in Cr, has been introduced to alterations in renal function.11 When the more se- describe early damage with intrinsic renal disease.19 lective COX-2 NSAIDs were initially introduced, This predominantly tubular damage may be charac- there was hope that they would be more sparing of terized by proteinuria, microscopic hematuria, glu- renal function than nonselective COX inhibitors. cosuria, increased urine sodium and chloride However, it is now recognized that these newer concentrations and excretion, increased urinary en- NSAIDs provide little benefit of limiting renal dam- zyme activities, and detection of novel biomarkers of age; thus, all NSAIDs should be used sparingly in tubular epithelial damage in urine (kidney injury compromised foals.12 molecule 1 and others). Examination of urine sed-

AAEP PROCEEDINGS ր Vol. 57 ր 2011 329 MEDICINE II iment may also reveal hyaline or granular casts. 5. Post-Renal Failure These urinary changes can develop a few days before Azotemia arising from disruption of the urinary onset of significant azotemia. tract typically occurs in the face of nearly normal With both pre-renal and renal azotemia, acute kidney function, but failure to eliminate urine leads changes are better assessed by the comparatively to progressive abdominal distension and electrolyte greater increase in Cr than BUN, due to the larger alterations. Hyponatremia, hypochloremia, and size of Cr that slows its diffusion out of the extra- hyperkalemia develop with “mixing” or “dialysis” of cellular fluid (ECF) space. Thus, following changes the expanded peritoneal fluid compartment with the in Cr over time is more reliable for assessment of remainder of the ECF compartment, including changes in renal function than is monitoring BUN. plasma.24 Again, because Cr does not diffuse out of However, it warrants emphasis that increases in Cr the ECF compartment as rapidly as urea, finding a are insensitive for detection early changes in renal peritoneal fluid Cr to serum Cr ratio Ͼ2 is the clin- function (GFR must decrease by 75% or more before icopathologic test of choice to confirm uroperito- azotemia develops). Further, an occasional foal neum. However, this test is being performed less may have a more marked increase in BUN than Cr, frequently than in the past because detection of a and, in such cases, upper intestinal ulceration with large volume of hypoechic fluid within the abdomen blood loss into the intestine should be considered as via transabdominal ultrasonography is essentially a a potential cause for the increase in BUN. Next, pathognomonic finding in foals with electrolyte alterations expected with uroabdomen. another simple question to ask is whether or not The classic case of uroperitoneum occurs in 2- to acid-base status and serum electrolyte concentra- 3-day-old colts that develop abdominal distension tions are normal. These parameters typically re- consequent to a dorsal bladder wall tear sustained main normal with pre-renal azotemia, whereas as they pass through the pelvic canal with a full alterations are common with intrinsic renal failure bladder.24 However, silent uroabdomen can also (hyponatremia, hypochloremia, hyperkalemia, and develop in compromised neonates in intensive care metabolic acidosis). A final hallmark of tubular units, especially when they are unable to stand and damage associated with AKI and intrinsic renal fail- void urine normally. Uroabdomen in these foals ure is loss of concentrating ability. Urine of af- may develop as a consequence of bladder distension fected foals is typically hyposthenuric (specific and leakage/rupture or can be due to a small leak in Ͻ Ͻ 25,26 gravity 1.008 and Uosm 300 mOsm/kg). association with sepsis of the urachus. Uroab- With AKI and intrinsic renal failure, it is impor- domen in these foals may not become a problem tant to determine whether or not affected neonates until 4 to 7 days of age and is often first detected as are oliguric (urine output Ͻ0.5–1 mL/kg/h) because an increase in free abdominal fluid during routine oliguric AKI carries a more guarded prognosis than transabdominal ultrasonographic monitoring of sick does nonoliguric AKI.11 However, most cases in neonates to assess intestinal motility and bladder neonates are nonoliguric, and these may only be size. At initial suspicion of uroabdomen, enough detected by finding a progressive increase in Cr with time may not have elapsed for electrolyte alterations serial serum biochemical analyses. Fortunately, to develop (or they may be attenuated by concurrent neonatal kidneys are forgiving, and treatment can IV fluid therapy), but uroperitoneum can be con- sometimes be successful with anuria/oliguria lasting firmed by comparing peritoneal fluid Cr to serum Cr. up to 72 hours. Dialysis, either peritoneal or hemo- Finally, another cause of “late onset” uroperitoneum dialysis, is also feasible in foals as compared with can be a ruptured ureter. Most ureteral leaks occur full-sized adult horses when anuria/oliguria per- near the kidney and may be associated with blunt 20,21 abdominal trauma during parturition or after sists. However, recent reports of peritoneal di- 27 alysis as a treatment for oliguric renal failure in birth. The author has seen several cases of ure- horses are not without controversy, as careful re- teral leakage in foals with multiple rib fractures, view of the reports reveals that urine output was not supporting birth trauma and possible delivery with well documented22 and that Cr had already begun to the mare in a standing position as potential risk factors. Urine initially accumulates more slowly in decline before dialysis was initiated.21 The main the retroperitoneal space until it ruptures into the challenge of treating patients with anuric/oliguric peritoneal cavity. Further, with unilateral ure- renal failure is not to control Cr; rather, it is to teral rupture, the bladder continues to fill from the maintain acid-base balance and serum electrolyte contralateral side and normal urination may still be concentrations within reasonable ranges while renal observed. tissue is repaired and urine production returns. Of interest, recent evidence in management of ARF 6. Congenital Disorders in people provides further support for cautious IV Anomalies of renal development reported in foals fluid support of compromised foals (so-called “run- include agenesis/aplasia, hypoplasia, dysplasia, and ning them dry”) because excessive fluid replacement polycystic kidney disease (PCKD).28 Although may increase intrarenal pressure and further com- present at birth, anomalies may not lead to azotemia promise restoration of renal function.23 and renal failure until later in life, especially renal

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Fig. 2. Ultrasonographic appearance of a normal left kidney of an approximately 50 kg neonatal foal acquired transabdominally with the probe placed on the left paralumbar fossa (left) or under the last few ribs and directed dorsomedially (right); length is ϳ10 cm and renal parenchyma is hypoechoic when compared with the spleen; the renal medulla is also more hypoechoic than the cortex. hypoplasia or PCKD. For example, the author di- or possibly larger than normal (supporting intra- agnosed PCKD as the cause of CKD in a 19-year-old uterine urachal obstruction or lack of detrusor tone). Arabian mare. Anomalies of the collecting system If the bladder is larger than 10 cm in diameter and such as ureteral ectopia do not typically cause renal urination is not observed within 30 to 60 minutes failure and azotemia unless complicated by obstruc- after this finding, a catheter should be passed to tion or ascending urinary tract infection. Mega- collect a urine sample and to empty the bladder. vesica, or a markedly enlarged bladder, has been Indwelling bladder catheters with closed collection described in several foals in association with sus- systems are being used more frequently in recum- pected urachal obstruction and can cause post-renal bent neonates and are certainly helpful in docu- failure and abdominal distension (due to the large menting rate of urine production. However, even bladder) without actual disruption of the urinary well-managed catheters are commonly colonized tract.29 with multidrug resistance bacterial spp.; thus, short-term use (Ͻ3 days) is the goal and prophylac- 7. Evaluation and Management of Azotemia tic antimicrobial treatment is warranted. When azotemia is detected in a neonatal foal, re- One of the hallmark treatments of azotemia is peating the physical examination may detect subtle supportive fluid therapy. However, the approach findings that may not have been appreciated during should err on the side of caution. For example, the initial exam. For example, mild edema or with pre-renal azotemia and spurious hypercrea- “looseness” of the skin in the axillary and inguinal tininemia, fluid support can often be limited to en- regions may be appreciated with oliguria, and foals teral milk feeding or close observation to ensure with hyperkalemia may have fine muscle tremors adequate nursing. With milk alone provided at that may be easier to feel than to see. Evidence of 10% or more of body weight daily, foals will be re- incontinence may support ectopic ureter, and moist- ceiving a fluid intake at a rate more than adequate ness of the umbilicus may support localized sepsis for maintaining hydration. Although adequate nu- that may lead to subcutaneous urine accumulation tritional support with enteral milk feeding can be and/or uroperitoneum. In addition to physical ex- accomplished in all neonates that tolerate milk feed- amination and a clinicopathologic database, abdom- ings, it is important to remember that foals will inal ultrasonography should be a standard part of produce dilute urine (specific gravity Յ1.005) when the work-up of neonatal foals. With regard to the fed either 10% or 20% of body weight daily as milk. urinary system, the first question to answer is However, they will produce a greater amount of whether or not the foal actually has two kidneys dilute urine when they are fed more. Thus, assess- that are of normal shape and size (about 5 ϫ 10 cm ment of body weight gain daily is a superior method for a 50-kg foal, Fig. 2).30 Foals that have nursed of assessing adequacy of either nursing or enteral well or that have been started on IV fluid support feeding, as compared with only measuring urine and are producing adequate urine often have mild specific gravity. When enteral feeding is not toler- distension (to 1–1.5 cm) of the renal pelvis (Fig. 3), ated well and/or when acid-base balance or serum but this should be a symmetrical finding in both electrolyte concentrations are altered, judicious IV kidneys. Next, the bladder should be imaged to fluid therapy support may also be required. A po- determine whether it is small (supporting oliguria) tassium-free IV fluid (0.9% saline solution) should

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Fig. 3. Ultrasonographic appearance of normal kidneys of equine neonates receiving IV ﬂuids showing distension of the renal pelvis to nearly 2 cm in diameter.

be used when significant hyperkalemia (Ͼ5.5 intervals and may still return to normal values over mEq/L) is present, whereas a polyionic replacement 1 to 3 months. fluid can be used when potassium concentration is In foals with oliguric ARF, judicious fluid therapy not elevated. The goal should be to limit fluid re- is even more critical to prevent volume overload. placement to maintenance to 1.5 times maintenance Although efficacy remains unproven, furosemide requirements (1.0–1.5 mL/kg/h), and patients on IV (1–3 mg/kg, q 2 hours, IV) may be used in an attempt fluids should be monitored twice daily for develop- to increase urine flow rate. If no effect is observed, ment of edema and body weight change. Urine pro- mannitol (0.25–1.0 g/kg, IV) has also been used as duction can also be monitored with an indwelling an osmotic diuretic but, again, supportive data are collection system, and central venous pressure lacking in foals, and this treatment has fallen out of (CVP) can be monitored via the jugular venous cath- favor in human medicine. Similarly, use of a dopa- eter placed for fluid administration (as the catheter mine infusion in an attempt to increase renal blood end is often near or in the right atrium). Ideally, flow is no longer recommended in human medicine CVP should be maintained below 10 cm H2O. Fur- because of the potential for development of arrhyth- ther, the enteral route, when it is working, can also mias and a lack of data substantiating improved be used for administration of sodium chloride, so- long-term outcome.31 Despite the lack of clinical dium bicarbonate, potassium chloride, or potassium evidence for treatment of anuric or oliguric ARF, bicarbonate. Once foals are tolerating enteral feed- continuous rate infusion of pressor agents, including ing well or are nursing adequately, they will have a dopamine, norepinephrine, or dobutamine, may be fluid intake that may be 3 to 5 times maintenance of benefit to foals with systemic hypotension, as part requirements, and there is little benefit of additional of the overall neonatal supportive care although the IV fluids. The resultant diuresis is generally ade- electrocardiogram (ECG) should be closely moni- quate for resolution of azotemia, as long as damaged tored during use of these drugs.32 Finally, perito- renal tissue undergoes repair. Thus, IV fluid ther- neal dialysis can be considered with refractory apy does not need to be continued until azotemia has oliguria and worsening azotemia. The goals of di- fully resolved and can often be stopped once Cr alysis are to both correct electrolyte alterations and concentration has stabilized at values Ͻ2.5 to 3 acid-base status along with controlling azotemia, mg/dL (ϳ250 ␮mol/L), although Cr concentration but a more guarded prognosis should always be is- should be measured again 1 to 2 days after discon- sued for owner consideration before this more inva- tinuing IV fluids to make sure that it is not increas- sive treatment is pursued. ing again. What is difficult (or impossible) to know Surgical correction of urinary tract disruption is at the start of therapy is what the final Cr will be generally the treatment of choice for uroabdomen, after repair of damaged renal tissue. Many cases although small bladder rents may heal with place- will have Cr return to values within the reference ment of an indwelling bladder catheter alone.33 range within 5 to 10 days, whereas others will be With uroabdomen, large volumes of urine in the discharged with persistent elevations in Cr. In the abdomen may compromise ventilation, and moder- latter cases, Cr should be monitored at monthly ate to severe hyperkalemia (Ͼ6.5–7.0 mEq/L) may

332 2011 ր Vol. 57 ր AAEP PROCEEDINGS MEDICINE II men is probably as important as ﬂuid therapy in overall management of hyperkalemia; thus, drainage should not be delayed while attempting to decrease serum potassium concentration. Once affected neonates have been stabilized and serum potassium concentration is Ͻ5.5 mEq/L, surgical correction of urinary tract disruption can usually be safely pursued.

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