Kidney Homeostastis

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Kidney Homeostastis by Mind Map: Kidney Homeostastis

1. Physiology

1.1. Acid Base Equilibrium -                                 Blood ranges in pH from 7.35 to 7.45. This delicate balance is maintained by the kidneys. The kidneys causes a reabsorption of bicarbonate ions and secretion of hydrogen ions into the tubular fluid

1.1.1. In acidosis, the tubular cells of the kidney reabsorb more bicarbonate and collecting duct cells secret more hydrogen ions with a marked increase in the buffer (NH3)

1.1.2. In alkalosis the kidneys lower rates of glutamine metabolism, and hydrogen ion secretion is decreased. Ammonium excretion is also reduced

1.2. Electrolyte Balance

1.2.1. ADH, angiotensin II, aldosterone and atrial natriatic peptide (ANP) are hormonal regulators that determine how much sodium and chloride are excreted from the kidneys

1.2.2. Renin converts angiotensin I to angiotensin II causing reabsorption of sodium in the kidneys. Angiotensin II stimulates aldosterone which also causes a reabsorption of sodium and a release of potassium. This retention of sodium creates a pull for the water back into the capillaries causing an increase in blood volume.

1.3. Blood pressure

1.3.1. Renal control of sodium and water that affect blood volume and consequently blood pressure

1.3.2. When blood volume is low, renin is secreted by the juxtaglomerular cells into the blood. This sets off a cascade that causes the release of ACE from the lungs which converts angiotensin I to angiotensin II. Angiotensin II causes constriction of the blood vessels resulting in an increase in blood pressure.

1.4. Total body volume & osmalality       Approximate loss and gain of 2500mL daily and kidney accounts for an average of 1500mL

1.4.1. Loss of water volume causes a decrease in blood pressure. This causes a release of renin by the kidney. Renin stimulates release of angiotensin II which alerts the hypothalamus to activate thirst sensors

1.4.2. ADH secretion causes an increase in fluid retention

1.5. RBC

1.5.1. The hormone erythropoeitin is secreted from the kidneys

1.5.2. Patients with kidney failure are often anemic

1.6. Glucose regulation

1.6.1. Gluconeogenesis by the kidney

1.6.2. Glucose uptake for kidney's functional needs

1.6.3. Resorption of glucose in the tubules

1.7. Hormone regulation

1.7.1. Release of renin,

1.7.2. Actions of ADH cause increase in diureses

1.8. Glomerular Filtration Rate (GFR)

1.8.1. Kidney receives approximately 20-25% of blood supply. The afferent arteriole feeds the glomerular capillaries and maintains the GFR, and blood exits via the efferent arteriole. This placement between the two structures maintains the blood flow needed

1.8.2. The afferent and efferent arteriole are innervated by the sympathetic nervous system, thus allowing the GFR to rise or drop when the SNS is stimulated, or when exposed to  vasoactive hormones and drugs such as a epinephrin and angiotensin receptor agonists respectively.

2. Treatment

2.1. Renal Replacement Therapy

2.1.1. Hemodialysis is the filtration of solutes in the blood outside of the body. Indicated in kidney failure, fluid overload

2.1.2. Continuous Renal Replacement Therapy slowly removes solutes and excess fluid 24 hours and 7 days a week. Controls electrolyte imbalance

2.1.3. Kidney Transplant

2.2. Pharmocologic

2.2.1. Thiazide Diuretics are most effective in those with normal kidney function. Inhibit reabsorption of sodium and chloride

2.2.2. Angiotensin Receptor Blockers work to block the effects of angiotensin to prevent salt and water retention, as well as constriction of blood vessels.

2.2.3. ACE Inhibitors - block the conversion of angiotensin I to angiotensin II. By blocking the conversion, there are decreased levels of angiotensin which constrict blood vessels and cause salt and water retention

2.2.4. Loop Diuretics - indicated for Fluid Overload. These inhibit the reabsorption of sodium and water in the loop of Henle by inhibiting the sodium chloride potassium pump.

2.2.5. Erythropoietin Stimulating Agents can be used to treat anemia in the patient with kidney injury along with iron supplemetns

3. Medical Diagnosis & Assesment

3.1. Assessment

3.1.1. Proteinuria - The increase in protein in urine indicates a problem with filtration in the kidney's tubular system.

3.1.2. Glomerular Filtration Rate - Measure of serum creatinine to estimate glomerular filtration rate

3.1.3. Renal Biopsies

3.1.4. Vascular Studies

3.1.5. Renal CT & MRI

3.1.6. Cystographic Studies

3.2. Diagnosis

3.2.1. Acute Kidney Injury (AKI) - is an abrupt reduction in kidney functions that lead to an increased concentration in Blood Urea Nitrogen (BUN) and serum creatinine. Pre-renal - caused by hypoperfusion of kidneys. Hypotension, renal artery stenosis and hypovolemia, and vasoactive medications that constrict the renal arteries are all common causes of pre-renal kidney injury. Intrinsic - caused by damage to the structural components of the kidney through inflammation and injury by toxins, infectious agents, or by prolonged exposure to pre-renal causes which can lead to necrosis through ischemia Acute Tubular Necrosis is the most common cause of AKI. This condition is marked by injury induced shedding of epithelial cells that block the tubules and cause leakage of filtrate through the damaged epithelium. Acute Interstitial Nephritis is usually caused by an immune reaction to nephrotoxic drugs such as NSAIDS. Antigens bound to these nephrotoxic drugs deposit in the interstium and cause an immune reaction. Contrast Induced Nephropathy can occur approximately 24 hours after contrast use (e.g. CT scan, angiograms). Although rare, conditions such as diabetes, heart disease, advanced age, and chronic kidney injury greatly increase the risk. Using a lower osmole contrast in a smaller dose, drinking water, and decreasing procedures in a 48 hour period have been considered potential safeguards for this reversible disease. Post-Renal - focuses on obstruction. Obstructions can be caused by benign prostate hyperplasia, structures, kidney stones (renal caliculi), pregnancy or blood clots. These obstructions cause an increase in the kidney system pressure with leads to a decrease in GFR, and decrease in sodium and water reapsorption.

4. Nursing Diagnosis & Interventions

4.1. Diagnosis

4.1.1. Fluid Volume Imbalance

4.1.2. Altered tissue perfusion

4.2. Assessment

4.2.1. Fluid management: Regular monitoring of intake and output IV Oral intake Urine output Wound and nasogastric drainage

4.2.2. Monitor lab results: BUN Serum Creatinine pH Electrolytes CBC

4.2.3. Assess the client for evidence of electrolyte imbalance: Cardiac Dyspnea Muscle Tremors Kaussmaul's respiration Tetany

4.2.4. Monitor respiratory status every 8 hours in case of pulmonary edema

4.2.5. Assesment of Patient risk factors Previous Kidney Issue GFR of less than 60 Advanced age, 60+ Diagnosis of sepsis Diabetes Mellitus Heart Disease Repeated exposure to nephrotoxic drugs

4.3. Interventions

4.3.1. Fluid restriction as instructed to prevent overload

4.3.2. Vital signs such as weight and orthostatic blood pressure taken daily