Renal Case Study

Renal Case Study Mr. L, 58yo male, admitted to the telemetry floor after becoming very SOB and a 5 pound weigh gain over the last 2 days. He has a past medical history of Type 2 DM, HTN, MI (2017) and had 2 stents placed and has been on dialysis since his MI. It is Saturday night and his last dialysis was Friday morning. He was at a graduation party for his niece today and admits to eating the chips and pretzels on the table and he had 2 beers. He is being admitted and is waiting for dialysis. Meds: Lisinopril 40mg Metoprolol 50 mg Clopidogrel 75mg daily ASA 81mg daily Calcium Carbonate 1 pill before each meal Cholecalciferol 600mg daily Insulin Glargine 25u in the evening Insulin Lispro 6u 15 minutes before each meal Hydrocortisone Cream twice daily as needed Loratadine every 48 hours as needed for itching 1. Identify the triggers which caused the fluid overload and explain why? Mr. L became fluid overloaded because he missed his dialysis session and consumed chips and pretzels which are high in salt along with 2 beers at the graduation party. In kidney failure, sodium and fluid are not effectively excreted, so excess intake leads to fluid retention. Dialysis is needed to remove that excess. The missed dialysis plus high sodium intake caused water retention, leading to shortness of breath and weight gain. 2. Write out the anticipated neuro/CV/Resp/GI/GU/skin physical exam on this patient? Neuro: confusion or lethargy from uremia Cardio: Hypertension, jugular vein distension, peripheral edema Respiratory: Crackles in lungs, shortness of breath GI: Nausea, anorexia, maybe vomiting GU: Likely very little to no urine output (anuria/oliguria) Skin: Pale, dry, itchy skin with signs of scratching (uremic pruritus) 3. Mr. L receives iron and erythropoietin during dialysis. Explain why this happens? In chronic kidney disease, the kidneys stop producing erythropoietin, the hormone that stimulates red blood cell production. This leads to anemia. Erythropoietin injections help boost RBC production. Iron is given to support hemoglobin synthesis and ensure the erythropoietin works effectively. 4. Why is Mr. L on Lisinopril, Metoprolol, ASA and Clopidogrel Lisinopril: ACE inhibitor for blood pressure and kidney protection Metoprolol: Beta-blocker for BP and post-MI cardiac protection ASA (Aspirin): Antiplatelet to prevent clots and protect stents Clopidogrel: Antiplatelet to prevent stent thrombosis and future cardiac events 5. Why does Mr. L take calcium carbonate and cholecalciferol? Calcium carbonate: A phosphate binder taken with meals to prevent phosphorus absorption, which builds up in CKD and causes bone problems. Cholecalciferol (aka Vitamin D3): Helps absorb calcium and regulate bone metabolism, CKD causes vitamin D deficiency due to impaired kidney activation of the vitamin. 6. Explain the electrolyte abnormalities which he may experience? a. Potassium – Hyperkalemia → kidneys can’t excrete K⁺, which can cause dangerous cardiac arrhythmias b. Calcium – Hypocalcemia → kidneys can't activate vitamin D, so calcium absorption drops c. Phosphorus - Hyperphosphatemia → phosphate is retained, contributing to bone disease d. Magnesium - Can be elevated mildly but usually less critical unless patient takes magnesium containing meds e. Sodium - can be normal or low if fluid overloaded (dilutional hyponatremia) 7. Mr. L. receives dialysis and his symptoms resolve. Provide the patient teaching the nurse will give to him regarding diet and fluid intake? • • • • • • • Fluid restriction based on dialysis schedule and output. Low sodium diet; avoid chips, pretzels, and processed food Limit potassium rich foods like bananas, tomatoes, oranges, melons Limit phosphorus ex. dairy, beans, sodas, nuts Avoid caffeine, it worsens dehydration and can irritate kidneys Encourage daily weight checks to monitor fluid retention Stress importance of not skipping dialysis 8. Explain how Mr. L past medical history contributed to him ending up on dialysis? Hypertension and Type 2 diabetes are the leading causes of chronic kidney disease due to long term damage to glomeruli and vasculature. Mr. L’s MI in 2017 and resulting hypotension likely caused further injury. These chronic conditions led to progressive kidney dysfunction which resulted in end stage renal disease and so the need for dialysis. 9. When he had his MI in 2017, he had an episode of hypotension and bradycardia in the cardiac cath lab when getting his stent. He was resuscitated but then had acute kidney injury. What are the factors which caused this AKI (think pre/intra/post)? Pre-renal: Hypotension and decreased perfusion during the MI and in the cath lab Intra-renal: Possible contrast-induced nephropathy and ischemic injury from low perfusion Post-renal: Unlikely, but obstruction should always be ruled out 10. What are the stages of AKI? Onset Phase • Triggered by events that reduce kidney perfusion (e.g., hypotension, ischemia) • Renal blood flow drops to <25% of normal • Tissue oxygenation is reduced • Urine output < 0.5 mL/kg/hr • Duration: Hours to a day Oliguric Phase • Urine output < 400 mL/day • Increase in BUN and Creatinine • Fluid & electrolyte imbalance from retention and acidosis • Duration: 8–14 days or longer, depending on cause and dialysis status Diuretic Phase • Begins when AKI starts to resolve • Tubular scarring occurs • GFR increases • Urine output > 400 mL/day • Risk of electrolyte depletion from high-volume water loss • Duration: 7–14 days Recovery Phase • Edema decreased, F&E balance returns • GFR recovers to 70–80% of baseline • Can take several months to a year