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A comprehensive overview of chronic kidney disease (ckd) and acute kidney injury (aki), covering their causes, stages, symptoms, diagnostics, and treatment. It includes detailed explanations of prerenal, intrarenal, and postrenal injury, as well as the stages of aki and ckd. The document also features exercises and questions to test understanding and reinforce learning.
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Sudden decrease in renal function that will lead to the buildup of waste (creatinine and urea) in the blood, fluid overload, and electrolyte imbalances. CAN BE REVERSED AKI RF Advanced age Autoimmune disease Uncontrolled HTN DM Certain cancers Heart, liver, and kidney disease Antibiotics Heavy metals Chemotherapy Iodinated IV contrast Dye Previous Play Next Rewind 10 seconds Move forward 10 seconds Unmute 0: / 0: Full screen
Brainpower Read More What is prerenal injury? Issue with perfusion to the kidneys (an injury BEFORE the kidneys) No physical problem with the kidneys themselves Such as MI or HF (heart muscle damage and can't pump enough to the kidneys) Massive bleeding, dehydration, ascites, burns, hypovolemia What is intrarenal injury? Damage to the nephrons of the kidney (injury WITHIN kidney) Nephrotoxic drugs - NSAIDs, Antibiotics (aminoglycosides), chemo drugs, contrast dyes used in procedures Infection (UTI or glomerulonephritis) Injury toxins Prolonged ischemic injury What is postrenal injury? Blockage in the urinary tract after the kidneys to the urethra (injury found AFTER the kidneys) Prevents urine from draining from the kidneys Such as renal calculi (kidney stones), enlarged prostate, bladder doesn't empty full d/t neuro damage (stroke), strictures, tumors Stage 1 Initiation AKI a cause creates injury to the kidney and then signs and symptoms start to appear which leads to the next stage. This stage lasts a few hours to several days. Stage 2 Oliguric Stage AKI some patients skip this stage and go straight into the diuresis stage Urine output will be less than 400 ml/day or <30ml per hour Glomerulus Is not filtering the blood properly Decreased: GFR, sodium, calcium Increased: BUN, creatinine, K, fluid in the body, phosphorus, urine concentration May experience metabolic acidosis d/t decrease in excretion of hydrogen ions. This may last a week to 2 weeks - important that this stage is as short as possible to prevent long term kidney damage Stage 3 Diuresis AKI
Nephrons cannot concentrate urine but they can filter out waste (high levels of urea) Pt will be voiding an excessive amount of urine 3-6 L per day due to osmotic diuresis Pt may experience hypokalemia low specific gravity Last a week to 3 weeks Treatment during this stage: Strict I&Os Daily wt Monitor for s/s of dehydration Hypovolemia, Hypotension Stage 4 Recovery AKI Starts when GFR returns to normal and kidney function returns to normal All levels and urine output normal This stage can last a year or more it depends on the amount of damage done to the kidney and pt age Some pt unable to get to this stage and go into CKD. S/S of AKI Decreased urine output Fluid overload Increase in wt HTN Distended neck vein Bounding pulse Neuro changes Itching Diagnostics for AKI BMP High K and phosphate Low calcium, sodium High BUN and creatinine ABG metabolic acidosis Urinalysis Show proteinuria, hematuria, and casts High concentration Imaging studies To show renal blood flow and identify cause AKI treatment Reversible with prompt treatment Manage symptoms
Address underlying cause Combo of Fluids Diuretics Nutritional support - low protein diet (bc urea is a waste product from protein breakdown in the liver), restrict K foods Monitor fluids, electrolytes, and waste products of metabolism May give kayexalate to remove K from body Monitor EKG (tall peaked T-waves, Wide QRS and prolonged PR interval) Lung sounds (crackles) Strict I&Os - daily wts Swelling Dialysis CKD It is a significant decline in kidney function that happens over a long period of time that leads to the build up of waste, water, and electrolyte imbalances in the body. CKD is irreversible. CKD stages Stage 1: Kidney damage with normal renal function GFR >90 but with proteinuria 3 months or more Stage 2: Kidney damage with mild loss of renal function GFR 60-89 with proteinuria 3 months or more Stage 3: Mild to severe loss of renal function GFR 30- Stage 4: Severe loss of renal function GFR 15- Stage 5: End stage renal disease GFR < What hormones do the kidneys produce? (3) EPO (erythropoietin) This helps create RBCs in the bone marrow. With CKD this hormone decreases and leads to anemia Renin Plays a role in increasing blood pressure. In CKD the glomerulus is filtering less water and the kidneys think the blood pressure is low, so it releases renin, which in turn increases blood pressure even more. Vitamin D
Plays a role in helping the body reabsorb calcium from the food we eat. In CKD, the activation of vitamin D is diminished and this leads to lower calcium levels ( hypocalcemia ). CKD causes High blood pressure (hypertension): constant high pressure on the artery wall that supplies the kidneys causes damage. Therefore, less blood reaches the kidneys and the nephrons can't function properly. *Diabetes Mellitus: uncontrolled hyperglycemia causes glucose to stick to arteries walls, which damages the blood supply to the kidneys. Acute kidney injury Polycystic kidney disease: genetic condition where cysts grow in the kidneys Infection Nephrotoxic drugs: NSAIDS, aminoglycosides, chemo therapy drugs, contrast dyes for testing procedures CKD treatment in early stages Controlling blood pressure and glucose level Medications for hypertension that help protect the kidneys, such as ACE inhibitors "pril" or ARBs "sartan" - also for pt with DM Monitoring GFR and blood pressure regularly CKD treatment in advanced stage Dialysis Kidney transplant Diet changes Uremia what to look for! Safety: patient may be confused, assess neuro status Itching: due to deposits of urea crystals on the skin via the sweat glands. It looks like frost on the skin and is called “uremic frost” Low protein diet: urea is a waste product of protein breakdown (patient doesn’t need any more urea). However, patient needs some protein to prevent muscle wasting. Assess for kussmaul breathing was is deep/rapid breaths from the acid building up in the blood (metabolic acidosis). This type of breathing is a compensatory mechanism by the respiratory system to increase the blood’s pH. Treatment for CKD Monitor for signs of anemia, hyperkalemia, hyperphosphatemia, hypocalcemia, hypermagnesia, and low UOP and fluid overload
Monitor intake and output (strict) Daily weights Assess swelling and lung sounds "crackles" Monitor blood pressure Low sodium diet