Renal Replacement Therapy MCQs

Digital sub periosteal resorption is classical of Osteitis fibrosa cystica of hyperparathyroidism. In CKD secondary hyperparathyroidism may progress to tertiary hyperparathyroidism. The series of events that happen in CKD is: Declining GFR leads to reduced excretion of phosphate and thus, phosphate retention The retained phosphate stimulates increased synthesis of both FGF-23 by osteocytes and of PTH and also stimulates growth of parathyroid gland mass PTH production is stimulated by decreased levels of ionized calcium, which in turn, result from decreased levels of renal calcitriol production with reduced kidney mass and suppression of calcitriol production due to phosphate retention and elevated levels of FGF-23, which also increases degradation of calcitriol. Reference: Harrison's Principles of Internal Medicine, 21 st edition, Ch:311, Pg:2313

Referring to the above question, we can clearly say that this patient is suffering from adynamic bone disease. Note that the calcium and phosphorous given here are in mmol/l. Ca value has to be multiplied by 4. So the Ca is 11.6mg/dl. Phosphorous has to be multiplied by 3. So the value is 6mg/dl. Aluminium deposited can cause osteomalacia like picture and is seen with use of aluminium as phosphate binder and Al in dialysate. Osteitis fibrosa cystica is severe secondary hyperparathyroidism. An increase in plasma cells cause hypercalcemia and hypophosphatemia Reference: Harrison's Principles of Internal medicine, 21 st edition, Ch:410, Pg:3181, 3182.

The question deals with the management and prognosis of Lupus Nephritis. HCQ should be in the management of allclasses of lupus nephritis. Class I and II should be treated mainly based on the extra renal manifestations. Class III and IV are the proliferative and serious forms and require aggressive immunosuppression with high dose glucocorticoid with either MMF or Cyclophosphamide. Isolated Class V presents with proteinuria alone and has got better outcome than class IV. But class V often co exists with class III and IV. Class V with nephrotic range proteinuria should be treated with immunosuppression, usually steroid with calcinurin inhibitors. Reference: Harrison's Principles of Internal Medicine 21st edition Ch:356 Pg:2739-2747 KDIGO guidelines

Acute monoarthritis with fever should raise the suspicion of septic arthritis especially in immunosuppressed patients. Reference: Harrison's Principles of Internal Medicine 21st edition, Ch: 370, Pg: 2845

This is patient has low C3 levels. So we may tend to think of PSGN. But here, there is no history of sore throat or preceeding streptococcal illness. Another point against PSGN is the presence of nephrotic range proteinuria which is very rare in PSGN. So the answer is MPGN. We should know that mesangiocapillary glomerulonephritis and membranoproliferative glomerulonephritis are the same and is just a histologic diagnosis and noy etiologic. Reference: Harrison's Principles of Internal Medicine, 21 st ed, Ch: 314, Pg: 2341.

EPO therapy may lead to hypertension and seizures. Other side effects of treatment with erythropoietin include hyperkalaemia in uraemic patients, increased PCV, thrombocythemia, shunt thrombosis, iron deficiency and urticaria. Reference: Harrison's Principles of Internal Principles, 20 th edition, Ch:305, Pg: 2117, 2118, 393, 499, 729

Kidney Donor Profile Index(KDPI) is a score designed to estimate the risk of graft survival, ranging from 0-100%. Lower KDPI is associated with lesser chance of rejection. KDPI of Living donor transplants do well than deceased donor transplant. Immunosuppression is not required for identical twin and combined kidney-bone marrow transplant. Induction therapy will be done with depleting agents like ATG or Alemtuzumab or non-depleting agents directed against IL2 receptors to reduce the risk of acute rejection. Reference: Harrison's principles of internal medicine, 21 st ed, Ch: 313, Pg: 2325-2328.

Cyclosporine can cause HUS in renal transplant recipients, especially in those also receiving rapamycin, which increases tissue concentrations of ciclosporin. Drugs causing thrombotic microangiopathy: Calcineurin inhibitors Mitomycin C Clopidogrel Gemcitabine Proteasome inhibitors(Bortezomib) Oral contraceptives Interferon Tacrolimus and Sirolimus These drugs cause direct endothelial damage and is dose dependent. Antibody mediated TMA can occur with Clopidogrel, Quinine. It is dose independent. Reference: Harrison's Principles of Internal Medicine, 21 st edition, Ch: 317, Pg: 2365.