Q.550. What are the strategies to minimize dialysis-induced hypotension in the elderly?

 

HEAMODIALYSIS

Q.550. What are the strategies to minimize dialysis-induced hypotension in the elderly?

1)   Frequent assessment of D.W.                                                   

2)   Avoid excessive inter-dialytic Wt. gain (<5 % body Wt.)

3)   Avoid anti-H.T. drugs prior to DX or altogether.

4)   Reduce intake of narcotic analgesics & sedative hypnotics

5)   No heavy meals on, or just prior to DX.

6)   Increased hematocrit to 33%

7)   Evaluate for silent pericardial effusion

8)   Use Dzt sod. of >140 meq/L

9)   High Dzt calcium.

10) Use bicarbonate DX. (esp. é high QB)

11) Prox. O2, esp. é cardiac or respiratory dis. & preDX PaO2 of <80mmHg

12) Use biocompatible membrane

13) In selected ptn, use a cool Dzt (34°C!!).

14) Use DX machines é UF controls

15) Use sequential UF-DX; occasionally needed when high UF rates are retired.

16) Ameliorate risk f.s for LVH (anemia, hyperpara., aluminum overload)

17)Improve nutritional status & hypoalbuminemia if present .

Q.551. What is the chance for women on dialysis to be pregnant?   

A. Only 0.5 % of women in childbearing period can conceive each year, from which 30 % ⮞ Surviving infants. Infants us. premature & small for gestational age. Infertility is the role in women with ESRD, but if pregnancy occur⮞ increased the dose of DX. (daily dialysis).

Q.552. What is the importance of nutritional status assessment as an indicator for RRT?

A. According to recent K/DOQI guidelines, RRT should be initiated é evidence of malnutrition in advanced CKD. Ptn develops anorexia & decreased protein intake despite efforts to improve his nutritional status. If malnutrition develops before RRT start  Decreasd long-term survival & potential for rehabilitation.      

Q.553. What markers commonly used for detection of malnutrition in advanced CKD?

A. Markers commonly used for detection of malnutrition in advanced CKD:

(1) Anorexia, nausea & vomiting & Wt. loss.

(2) Subjective global assessment.

(3) Low albumin & pre-albumin: Albumin: Correlate well é protein stores. Pre-albumin⮞ shorter ½ life & change rapidly é nutritional changes. (🠟 13 mg/dl = malnutrition).

(4) Decreased dietary “protein” intake< 0.8 g./kg. or nPNA< 0.8 g/kg/d.= Malnutrition.

(5) Abn. “anthrobometric” measurements: rapid & reproducible method for evaluation of body fat & msc. mass (referred to standard for healthy adults). 

(6) Abnormally low pl. Cr.: pl. Cr. reflects muscle mass. Pl. Cr.<10 mg/dl. at the start of DX.= malnourished (USRDS, U.S. Renal Data Association).

(7) Other markers: Cholesterol, transferrin & Somatomedin C.

Malnutrition shoudld be  👉  Strong Indicator for start of DX. in CKD.      👆 

Q.554.What are the applied measures to reduce B2 -micro-globulinemia in ESRD?

A. K/DOQI (2003) for management of B2 –microglobuli amyloidosis (A.B2M):

1)   Screening for B2.M, incl. measuring of s. level of B2.M, is NOT recommended.

2)   Ptn. with/at risk for AB2.M, non-cuprophane high flux Dzer.s should be used.

3)   No currently available ttt. (except R.TX.)🠞 Stop dis. progression or Sm.tic relief.

4)   R.Tx.: should be considered to stop dis. progression/Sm.tic relief. in ptn. é B2M.

UK Renal association(2007):     

1.    Ultrapure water ☜ shd be regarded as standard.

2.    High flux synthetic & modified cellulose dzer, justified for cost/benefit ratio.

3.    Currently:No available evid. to support routine use of H.F. & HDF in ESRD.

4.    Balance of evidence: Use DX. regimen promoting removal of middle molecule in ch. DX.(> 3.7 y) or predicted to be ch. ptn. [Age, HLA Ssz, recurrent dis. etc].  

v High flux membranes🠟 B2M by diffusion/convection & adsorption.

v HDF 🠞Higher clearance of B2.M by convective removal.

v 🠝frequency & duration of DX. 🠞🠟B2.M.

Q.555. How to manage secondary hyperparathyroidism & mineral metabolism in dialysis patients?  What are the indications of parathyroidectomy (Pec.)? 

A. Management of secondary hyperpara. & mineral metabolism abnormal in DX.:

v  Maj. f.s responsible for stimulating parathyroid gland in R.F.:† {hypocalcemia, low 1,25-dihydroxyvit. D & hyperphosphatemia}.

v  If physiologic abnormal are uncorrected, R. bone dis. will developed:† [weakness, fractures, bone & msc. pain & avascular necrosis, mostly in DX.]. Along é R. osteodystrophy, 2ry hyperpara. is ass. é diso. of mineral metb., mainnly abn. in Po4 & Ca. in addition to increased risk of all-cause & CVS, M.R. é disorder of mineral mtb.

v  So, keep i.PTH (2nd generation PTH assay): 150-300 pg/mL (80-160 pg/mL é Bi-PTH assay), Po4: 3.5-5.5 mg/dL (1.13-1.78 mmol/L) & corrected Ca:(8.4-9.5 mg/dL (2.10-2.37 mmo l/L).  

v  Current management of 2ry hyperpara. in DX involves: combination of Po4 binders (either Ca or non-Ca containing binders), vit. D analogues & calcimimetic.  

v  Ptn. é increased i.PTH, the general strategy is to dcreased s. Po4 to normal, limit excessive Ca. loading, avoid high dose active vit. D analogue, decreased. vit. D analog dose in ptn. é suppressed PTH, use a calcimimetic to help lower PTH, prevent progression of parathyroid dis., maintain bone health & prevent fractures.  

v  Ptn é increased PTH.: stepped approach to management of hyperpara. & bone mineral abnormality. This approach requires a complex balance of 4 drugs, namely {Ca-containing binders, non-Ca binders, calcimimetics & vit. D analogues}.

Aspects of suggested approach include:

v  Initial focus in managing 2ry hyperpara. is†management of hyperphosphatemia é diet and/or Po4 binders. Sp. interventions us. based é s. Po4 & Ca levels.   

v  Next: decide whether Po4 binder is sufficient or calcimimetic/vit.D analogue should be added, based é Ca, Po4 & PTH measured during starting Po4 binder.   

v  Finally: adjust Po4 binders “doses”, active vit. D & cinacalcet to target values.

A. Indications of parathyroidectomy:

                           I.        Sever Hyperparathyroidism:

(1) With persistent hyperphosphatemia.

(2) Unresposive to Calcitriol & Calcium.

(3) Renal Tx. candidates.

(4) With sev. hypercalcemia.

(5) Evidence of metastatic calcifications.

                         II.        Calciphylaxis with evidence of hyperpara.

                       III.        Severe pruritus, only if additional evidence of hyperpara.

N.B. Patients é CKD 5 on Dx, s. phosphorus should be maintained between 3.5-5.5 mg/dL bec. Sustained hyperphosphatemia † SHPT thr. sustained low s. Ca. PO4 binders are considered 2^nd-line therapy to control s. phosphorus and/or PTH following failure of dietary posphorus restriction. Although PO4 binders hv bn shown to decreased s. phosphorus, there’s no evidence tht this hs a direct effect on lowering s. iPTH in dialysis ptns., or dcr. morbidity & M.R. associated é SHPT. Vit. D sterols are considered first-line therapy in CKD DX ptn. é sust-ained increase s. iPTH. In addition to active vit. D sterols, calcimimetics may be used to treat high s. iPTH in CKD ptn. on DX. who have SHPT. Pec. should be considered in ptn. who do not achieve target s. iPTH, Ca+, PO4, or Ca+-PO4 cx. foll. trial of cinacalcet. Pec. should also be considered é sustained levels of iPTH > 800 pg/mL, or for é sustained levels > 470 pg/mL in whom target levels of s. Ca+, PO4, or the Ca+-PO4 cx hv bn achieved (Medscape).