Nephrology 6: CKD (Rapid Review)

Hi, Dr. Griffin. And I'm Dr. Taylor. Welcome to the evidence of the bedside rapid review series. Today we are doing a high yield rapid fire on chronic kidney disease. Let's get right into it. Question one. What is the strict minimum time requirement to diagnose chronic kidney disease based on abnormal kidney structure or function? It must be present for at least three months. Anything shorter strictly falls under acute kidney injury or acute kidney disease, so you need that time to prove it's chronic. Question two. Estimated GFR and the degree of albuminuria. The evidence shows this dual algorithm is critical because it predicts which patients are at the highest risk for progression to end stage kidney disease. Nailed it. Question three. In healthy adults over age 30, what is the average annual rate of EGFR decline? Approximately one millimeter per minute per 1.73 meter squared per year. Those with risk factors like diabetic kidney disease or heavy protonuria will decline much faster. Makes sense. Question four. What is the most common cause of death for patients with CKD stage G3 before they ever reach advanced CKD? Cardiovascular disease or infection. It's a key point because less than 10% of patients with stage G3 actually progress to end stage kidney disease. So bring statistic. All right. Question five. How does the literature temporarily define acute kidney disease compared to AKI and CKD? It is an acute reduction in EGFR persisting from 7 to 90 days. CKD strictly requires that impairment to persist beyond that 90 day mark. Spawn. All right. I'm taking the baton for set two. Shipping focus to diagnosis and initial management. Question six. A patient with an EGFR of 45 has bilateral shrunken kidneys less than 9 centimeters on ultrasound. Should a kidney biopsy be performed? No, shrunken kidneys indicate chronic irreversible disease. So a biopsy will absolutely not alter your clinical management. Exactly. Question seven. According to KDI GO, at what albumin to creatinine ratio is an apology referral strictly indicated? Consistently greater than 700 milligrams per gram or greater than 300 milligrams per gram if it's combined with the material. Perfect. Question eight. What four variables are included in the kidney failure risk equation to predict progression to end stage kidney disease? Age, sex, EGFR and albuminuria? Integrating this specific equation heavily improves clinical decision making over relying on EGFR alone. Right. Question nine. A 45 year old with CKD not on dialysis has a 10 year ASCVD risk of 12 percent. What lipid lowering therapy is indicated by KDI GO? A set. The literature states it's indicated for all adults 18 to 49 with non dialysis CKD and an estimated risk of coronary death or nonfatal MI greater than 10 percent. Good. Question ten. Should statin therapy be initiated in a patient who has just started a hemo dialysis for ESKD? No. It shouldn't. Large trials have consistently failed to demonstrate any mortality benefit for initiating statins in dialysis dependent patients. Exactly right. Okay. I'm jumping back in for set three. We're moving to mineral and bone disorders, question 11. In early CKD, which hormone rises first to induce phosphaturia before parathyroid hormone activates? Fibroblast growth factor 23 or FGF 23. It rises early in stage G3A CPD to compensate for the reduced phosphorous excretion. Yep. Question 12. What specific effect does FGF 23 have on vitamin D metabolism? It directly downregulates one alpha hydroxylase in the kidney. This completely inhibits the synthesis of active 1025 dihydroxy vitamin D. A crucial mechanism. Question 13. A patient with stage 4 CKD has elevated PTH, low calcium and high phosphate. What type of hyperparathyroidism is this? Secondary hyperparathyroidism. This is the classic physiological response to hypercalcemia and hyperphosphatemia in advancing CKD. Spot on. Question 14. What is the mechanism of tertiary hyperparathyroidism in advanced CKD? Well, prolonged PTH stimulation eventually causes severe parathyroid hyperplasia. The glands autonomously secrete high levels of PPH that are just no longer suppressable by elevated calcium. Right, they go completely rogue. Question 15. Describe the classic radiographic findings of osteitis fibrosisistica. Superior steel bone resorption, which is most prominent at the flanges of the hands, and radiolucent brown tumors in the long bones. Classic board fodder. Absolutely. I'll take set 4, keeping the focus on management and osteoporosis. Question 16. Why are bisphosphonates strictly avoided in patients with adynamic bone disease? Because they inhibit osteoclast activity. This severely worsens the already markedly reduced rate of bone turnover seen in adynamic disease. Good. Question 17. Below what EGFR threshold are bisphosphonates generally not recommended for the treatment of osteoporosis? In EGFR, less than 30 to 35 milliliters per minute per 1.73 meter squared. Dinosumab can sometimes be used, but it requires extreme caution. Speaking of which, question 18, what is the FDA boxed warning regarding the use of Dinosumab in patients with dialysis dependent stage 5 CKD? It's heavily associated with severe hypocalcemia. This is a very dangerous complication that has directly led to hospitalization and death. Very true. Question 19. Which specific class of phosphate binders must be entirely avoided in patients with CKD due to toxicity? Aluminum-based binders. They carry a very high risk of aluminum toxicity, so non-calcium-based binders like several amour are preferred instead. All right. Question 20. Should calcitril be used to lower PTH levels in a patient with stage 3 ACKD who is not on dialysis? No. The evidence strongly suggests avoiding vitamin D analogs for lowering PTH and on dialysis patients, unless they have severe progressive hyperparthyroidism in stages 4 or 5. Makes complete sense. Let's transition to anemia and acid-base for set 5. Question 21. At what hemoglobin threshold should a Rithropoysis stimulating agents be considered in a patient with CKD? Only when hemoglobin concentrations fall strictly below 10 grams per deciliter. Exactly. Question 22. What is the serious boxed warning risk for administering ESAs to push hemoglobin levels above 11 grams per deciliter in CKD patients? There is an increased risk for serious cardiovascular events in stroke. Plus, there is absolutely no added benefit in physical functioning at those higher targets. All risk. No reward. Question 23. What iron indices targets does KDIGOS suggest maintaining for patients with CKD in anemia? A transparent saturation greater than 30 percent and a serum ferritin greater than 500 nanograms per milliliter. Inadequate iron stores are a massive contributor to ESA hyperresponsiveness. Right. You need the wrong materials. Question 24. Why should blood transfusions be aggressively minimized in patients with advanced CKD awaiting a kidney transplant? To prevent allosensitization to HLA antigens, sensitization significantly increases waiting times for compatible kidney transplants. Good. Question 25. What type of acid-based disorder is most commonly seen in early CKD due to impaired ammonia genesis? A normal anion gap hyperchloremic metabolic acidosis. As the GFR drops further, retention of unmeasured anions will eventually lead to an increased anion gap acidosis. My turn for set 6. Let's drill hyperkalemia and protinuria. Question 26. At what chronically low serum by carbonate level, does KDIGO suggest initiating alkaline therapy? Less than 18 milliliter per liter. Alkaline therapy should be titrated up to the normal range to actively prevent muscle and bone loss. Right. Question 27. Why should you avoid dual therapy with ACE inhibitors and ARBs in a patient with protinuric kidney disease? Because dual blockade increases adverse events like hyperkalemia and AKI without providing literally any additional cardiovascular or renal benefits. Exactly. Question 28. A diabetic patient with CKD has an albimen creatinine ratio of 400 milligrams per gram and is already on an ACE inhibitor. What medication class should be added? An SGLT2 inhibitor. The literature demonstrates clear renal protective actions and reduced adverse kidney outcomes, especially for patients with a ratio of 300. Great point. Question 29. A patient with CKD stage 4 on an ACE inhibitor develops hyperkalemia. Before discontinuing the ACE inhibitor, what should be trialled? You should try a low potassium diet, oral bicarbonate, or potassium binders like paramir. This allows the patient to stay on those crucial kidney protective agents as long as possible. Yep. Question 30. Which specific environmental exposure is associated with a carcinogenic plant toxin known to cause chronic kidney disease? Aristolachic acid. Routine care must include careful history taking an absolute avoidance of this environmental toxin. All takes at 7, hitting imaging, vaccines, and specific meds. Question 31. For a patient with an EGFR of 25 requiring eye-addenated contrast, what prophylactic measure is recommended by the review notes? Intervenous hydration with.9% saline before and after contrast administration, unless it is contraindicated by their volume status. Spanon. Question 32. Wish group of gadolinium-based contrast media carries the lowest risk for an effrogenic systemic fibrosis in advanced CKD. Question 32. GBCM. The American College of Radiology considers this specific group to have a very low to non-existent risk of NSF. Right. Question 33. Why should peripherally inserted central catheters or PICC lines be strictly avoided in patients with an EGFR less than 60? To protect the veins of the non-dominant arm, preserving central vein patency is absolutely critical for future arteriovenous fistula placement. Gotta save the lifeline. Question 34, which oral pain medications are preferred in CKD due to their shorter half-lives and hepatic elimination? Oxycodone, hydro-morphone, or tramadol? NSIs are strictly avoided due to the high risk of AKI. Exactly. Question 35. Which common class of psychiatric medication is contraindicated with tramadol? in a CKD patient. Selective serotonin re-uptake inhibitors or SSRIs, the combination poses a severe life-threatening risk of serotonin syndrome. A very dangerous combo. Absolutely. Okay, moving to set eight on transplantation. Question 36. At what exact EGFR threshold should a patient be referred to a kidney transplant center for evaluation? An EGFR of 15 to 20 milliliters per minute per 1.73 meters squared, or when the two-year risk for kidney replacement therapy exceeds 40 percent. Yeah. Question 37. What is the preferred first-line and a hypertensive drug class for kidney transplant recipients according to Kediago? Die-hydroperidine calcium channel blockers or ARBs. However, extreme care must be taken with calcium channel blockers due to drug interactions with calcium urine inhibitors. Right. They can spike the drug levels. Question 38. A kidney transplant patient presents with an acute rise in creatinine. A biopsy reveals two below interstitial nephritis and ureteral stenosis, which unique viral infection is likely responsible. Polyonvirus BK infection. This uniquely affects kidney transplant recipients and requires a very careful reduction in their immunosuppression. Good. Question 39. A transplant recipient is on chronic maintenance with tecrolitis, prednisone, and microphenolite. What is the most common malignancy risk they face? Non melanoma skin cancer. Regular dermatologic screening is highly recommended for all transplant patients. Question 40. Post transplant lymphoproliferative disorder is heavily associated with impaired t-cell surveillance and which specific viral infection. Epstein-Barr virus. Treatment generally involves immunosuppression reduction and therapies like Ritexamab. Excellent. All right. Nearing the end was set 9 on dialysis complications. Question 41. A patient who recently missed several dialysis sessions undergoes a high efficiency hemodialysis treatment. They quickly develop headache, nausea, blurred vision, and confusion. Diagnosis. Dialysis disequilibrium syndrome. It's caused by osmodically mediated fluid shifts that lead to cerebral edema. Terrifying but true. Question 42. What organisms most commonly cause peritoneal dialysis associated peritonitis? Grandpositive skin flora. Proper rigorous aceptic technique during catheter handling is by far the best prevention. Right. Question 43. A patient on hemodialysis presents with highly painful interrated necrotic skin lesions with angulated borders on their thighs. What is the diagnosis? Calcifal axis also known as calcific erymic arteriolapathy. It strongly predicts poor outcomes including sepsis and death. Definitely a bad sign. Question 44. What common oral anticoagulants should be avoided in dialysis patients because it's a known risk factor for developing calcifal axis? Warfarin. Direct oral anticoagulants or alternative strategies should be used instead to avoid tipping them over. Exactly. Question 45. A patient on hemodialysis complains of severe intractable peritose. Besides optimizing dialysis, clearance and emolience, which capa opioid receptor agonist can be administered. Deep like felon. It is administered directly with the dialysis treatment to significantly improve their quality of life. Huge for patient comfort. Oh for sure. All right. Final stretch. Set 10. Infections and cystic disease. Question 46. What is the recommended management for a dialysis patient with a tunneled catheter who develops severe sepsis and persistent bacteremia despite antibiotics? Immediate removal of the tunneled catheter. Leaving it in place risks devastating metastatic infection. Yep. Question 47. A patient who's been on hemodialysis for 10 years develops new onset, gross hematuria and flank pain. What malignant transformation must be considered? Renal cell carcinoma. It arises directly from acquired cystic kidney disease, which is highly common in longstanding ESKD. Spot on. Question 48. True or false, the evidence recommends routine screening for renal cell carcinoma in all patients with end-stage kidney disease. False. Screening is strictly individualized for patients with a longer life expectancy, such as those actively awaiting transplantation. Right. It doesn't make sense for everyone. Question 49. A kidney transplant recipient shows signs of focal segmental glomerulus sclerosis in the alegraph. Why must this be treated aggressively? Because FSGS recurrence in a transplanted kidney is associated with exceptionally high rates of graft failure. Exactly. Last one. Question 50. When is the only exception to the rule against administering the influenza vaccine within the first three to six months post-transplant? It may be administered within one month of transplant if there is an active influenza outbreak. Otherwise, patients mount a very poor immune response during early high dose immunosuppression. Nicely done. And that concludes the drill. I want to sincerely congratulate you, the listener, for making it through this intense rapid review session. Please remember to explicitly like, share, and subscribe to evidence at the bedside. Signing off.