Chronic renal failure in dogs pdf

This may need to be achieved with low doses of loop-diuretics authors suggest 0. The physiological response to fluids and underlying conditions are dynamic over time, thus fluid administration should be based on repeated assessment of cumulative fluid balance and hemodynamic status. Generally, hemodynamic status can be assessed using dynamic testing to evaluate fluid responsiveness 5. Interest in intravenous fluid therapy and its side effects has increased in recent years.

In addition, the role of chloride and its detrimental effect on kidney function has garnered much attention 7 — Much of the research has focused on fluid therapy in the resuscitation phase, in which people receive large amounts of fluid over a short period of time. In reality, hospitalized people receive fluids and electrolytes for other reasons including maintenance therapy, medications, and replacement for existing or ongoing losses.

This is achieved via filtration of the circulating blood into ultrafiltrate from the plasma, selective reabsorption from tubular fluid into peritubular capillary blood, and selective secretion from peritubular capillary blood into the tubular fluid.

Glomerular filtration net ultrafiltration pressure is determined by the difference in hydrostatic and oncotic pressure gradients between the glomerular plasma and the filtrate in Bowman space. Maintaining a normal GFR is dependent on adequate renal perfusion.

Acute kidney injury AKI is defined as a rapid decline in GFR through the measurement of serum creatinine and urine output. There are inherent challenges with this definition as creatinine is poorly correlated with GFR at low levels of renal dysfunction Clinically, AKI is grouped into three etiologies: pre-renal, renal, and post-renal. Pre-renal azotemia is characterized by a decrease in GFR due to a decrease in renal perfusion pressure without damage to the renal parenchyma Post-renal causes of AKI are characterized by acute obstruction of urinary flow, leading to increases in intratubular pressure, impaired renal blood flow and inflammatory processes, and decreased GFR Renal azotemia is associated with a sudden onset of renal parenchymal injury, characterized by the kidneys inability to meet excretory, metabolic, and endocrine demands of the body.

AKI represents a continuum of renal injury from mild, clinically inapparent nephron loss to severe acute renal failure requiring renal replacement therapy. Intrinsic renal etiologies can be challenging to evaluate due to a wide variety of injuries that can occur to the kidney. In general, renal damage can be divided into four major structural groupings: the tubules, glomeruli, interstitium, and intra-renal blood vessels.

Tubular damage can arise from either ischemic injury decreased renal perfusion or nephrotoxic compounds exogenous and endogenous. Severe acute glomerulonephritis secondary to immune-complex disease causes glomerular damage. Interstitial damage can result from acute interstitial nephritis secondary to medications or infectious etiologies leptospirosis, pyelonephritis, etc. Lastly, vascular damage can occur secondary to injury to intra-renal vessels thrombosis, hypertension, etc.

Ischemia and nephrotoxic agents e. Renal tubular injury is associated with a decrease in GFR and is divided into different phases of AKI, which are directly related to the cellular events that occur during the injury and recovery process.

The initiation phase occurs when renal blood flow decreases, resulting in cellular ATP depletion and subsequent tubular epithelial cell injury.

These changes alter the ability of tubular epithelial cells and vascular endothelial cells to maintain normal renal function reabsorption and secretion , as well as up-regulate a variety of chemokines and cytokines to initiate an inflammatory cascade The extension phase is characterized by continued hypoxia following the initial ischemic event and an inflammatory response, most prominent in the outer medullary region of the kidney.

During this phase, vascular endothelial damage likely plays a key role in the continued ischemia of the tubular epithelium, as well as the inflammatory response. Cells in the outer medullary region undergo injury and death via necrosis and apoptosis The cellular injury in this region leads to the continual reduction in GFR, whereas cells of the proximal tubule in the outer cortex, where blood flow has returned, undergo cellular repair and improve morphologically The maintenance phase consists of cells undergoing repair, migration, apoptosis, and proliferation to reestablish and maintain cellular and tubular integrity.

The GFR usually remains stable at the level determined by the severity of the initial event. Cellular repair and reorganization results in slowly improving cellular function, setting the stage for improvement in organ function. Blood flow returns toward normal and epithelial cells establish intracellular and intercellular homeostasis During the recovery phase , cellular differentiation continues, epithelial polarity is re-established, and normal cellular and organ function returns Alternatively, renal repair can be maladaptive with inflammation, fibrosis, and vascular rarefaction leading to persistent cell and tissue malfunction and eventually chronic kidney disease AKI and chronic kidney disease CKD are increasingly recognized as related entities representing a continuum of disease The assessment of renal recovery is controversial with a lack of clear, defined parameters.

Partial recovery is defined as a fall in AKI grade. Recovery may occur early, after the insult within 7 days , or later, during the proposed period of acute kidney disease AKD , which is defined as AKI persisting for 7—90 days Lack of complete recovery in the first 90 days is defined as CKD.

Disruption of normal renal function impairs maintenance of homeostasis. A normochloremic high anion gap metabolic acidosis is common, due to inadequate excretion of organic and inorganic acids such as phosphate and sulfate. Hyperkalemia is also common when urine production is low and distal tubular secretion of potassium is impaired. Conversely, hypokalemia may develop with polyuria, as the high urine flow through the distal tubule enhances potassium secretion by maintaining a concentration gradient between the tubular cells and the ultrafiltrate in the tubule lumen.

Disorders of sodium are variable and depend on the degree of impairment of sodium reabsorption relative to water excretion. Because of impaired filtration and thus excretion of phosphate, leading to hyperphosphatemia, an ionized hypocalemia may develop acutely.

The physiological rationale for fluid administration in AKI and CKD is to optimize intravascular circulating volume, increase cardiac output and perfusion pressure, with the aim of improving renal blood flow, renal oxygen supply, and GFR Table 1. Hypotension is a strong risk factor for AKI, yet preserving systemic arterial pressure alone is not adequate for renal perfusion.

Renal tissue perfusion relies on the pressure in the post-glomerular arterioles, which is often much lower than the systemic MAP Conversely, fluid resuscitation beyond correction of hypovolemia does not increase the chances of renal recovery. Excessive fluid administration has been associated with the development of AKI, secondary to intrarenal compartment syndrome and venous congestion, attributed to the kidneys being encapsulated organs 24 , It is imperative to understand the physiological response to fluids and underlying condition related to AKI are dynamic, thus fluid administration should be based on repeated assessments of the patient and relevant biomarkers.

Overall fluid and hemodynamic status, using dynamic tests of fluid responsiveness are utilized to determine the need for additional fluid therapy 5.

The clinician is forced to walk a tight rope between too few fluids, which can lead to further progression of AKI from ongoing renal ischemia, and too much fluids leading to systemic complications and organ dysfunction.

Fluids are differentiated into crystalloids and colloids. Disregarding the impact of fluid overload, there is growing evidence that renal function is affected by the type of fluid and certain fluids are associated with an increased risk of AKI 24 , 26 , There is ongoing research as to which isotonic crystalloid, 0. The impact of chloride concentration on renal function has been researched in a Greyhound model, showing that increasing plasma chloride levels produce progressive renal vasoconstriction and decreased GFR.

These effects appeared to be related to tubular chloride reabsorption Both animal research and studies in healthy human volunteers suggest that hyperchloremia may lead to renal vasoconstriction, reduction in renal cortical tissue perfusion and glomerular filtration, along with longer periods of fluid retention compared with buffered crystalloids Clinical trials comparing various crystalloid fluids in critically ill people at risk of AKI have produced conflicting results 7 , 9 , 10 , Both found a significant reduction in the risk of major kidney events within 30 days, in the group treated with buffered solutions 9 , Despite these findings, the optimal fluid in people at risk of AKI has not been identified.

It is of the authors opinion that balanced crystalloids should be used for resuscitation and replacement therapy. Maintenance solutions hypotonic crystalloids are administered to meet the patient's basal requirements of water and electrolytes.

Specific maintenance solutions are commercially available but are far from ideal. Generally, the overall sodium and chloride load administered with maintenance and replacement fluids is not taken into consideration, even though these fluids account for a large portion of the daily fluid volume in these patients. Anemia may be treated with recombinant human erythropoietin. Dogs treated with Epogen have demonstrated resolution of anemia, weight gain, improved appetite, improved haircoat and improved sociability with their owners.

There are some risks associated with its use. Vitamin D calcitriol or 1,dihydroxycholecalciferol may be supplemented as Calcitriol synthesis is impaired with CRF. The benefits of supplementation are controversial. Calcitriol must only be used after hyperphosphatemia has been adequately controlled. Patient monitoring is an important part of continuing optimal treatment. Monitoring may include the following: serial body weight to determinations facilitate proper fluid therapy ; measurement of urine output; packed cell volume PCV and total plasma proteins will help monitor fluid load ; and serial determinations of serum biochemistry are necessary to determine if the animal is responding to treatment.

These determinants will help determine the proper fluid and drug therapy. Treatment may be required from three to five days, depending on the response and secondary causes. If treatment fails, dialysis or kidney transplant may be a treatment possibility.

Referral may be required for dialysis treatment. CRF may be progressive despite treatment. The prognosis for recovery of renal function depends on the severity of the renal lesions and the cause of CRF. Euthanasia may be considered for pets that do not respond to treatment. Follow-up Care for Dogs with Chronic Renal Failure Optimal treatment for your dog requires a combination of home and professional veterinary care.

Specific instruction for home therapy is determined by kidney damage. Follow-up can be critical and may include: Administer any veterinary prescribed medications as directed, and be certain to contact your veterinarian if you are experiencing problems treating your pet.

Some owners can administer subcutaneous fluid to their pets at home. Feed the diet recommended by your veterinarian. Provide your pet free access to fresh clean water at all times. Popular Posts.

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General Organic Compounds Screen. Glomerular Filtration Rate. Toxicology Sample Collection and Handling. Virology Expand. Staging of chronic kidney disease CKD is undertaken following the diagnosis of CKD in order to facilitate appropriate treatment and monitoring of the patient. Staging is based initially on fasting blood creatinine, assessed on at least two occasions in the stable patient. The patient is then substaged based on proteinuria and systemic blood pressure. Based on these categories, some empirical recommendations can be made about the type of treatment it would be logical to use for these cases.