HEMODIALYSIS

Q.566. What is the effect of underlying disease on the immune system in CKD patients?

 

HEMODIALYSIS

Q.566. What is the effect of underlying disease on the immune system in CKD patients?

A. D.M. is the most common cause of ESRD in UK & Europe. W.H.O. lists DM as a cause of secondary immunodeficincy disease. Hyperglycemia both innate & adaptive immune system é defect in chemotaxis, phagocytosis & cidal activity of lymphocytes & neutronphils. Other dis.: [Amyloidosis, M.M., autoimmune dis.] abnormalT-cell & A.B. function.

Q.567. How could the treatment of underlying disease affect the immune function in CKD?

1)   Im/m.: CNI, steroids, cytotoxic thpy & biologics im/m. effect of uremic syndrome. Different im/m. T-cell (CNI) & B-cell (MMF & rituximab) function. So, these effects should be discussed é ptn, é continuous monitoring (WBCs) & proper A.B. in time.

2)   Pph.:  removal of Ig. & complement  risk of infection (theoretical/ no evidence.).

Q.568 What are the recommended vaccinations in CKD & ESRD?

A. Most guidelines advocate the foll. vaccinations in CKD & ESRD:

1)   Hepatitis B;

2)   Pneumococcus,

3)   Influenza,

4)   Tetanus,

5)   Meningiococcus (serogroup B). Ptn. é CKD & ESRD are less likely to respond to these vaccination.

Q.569 What are the general recommendation in influenza/HBV vaccinations (Vcc.)?

(A) Influenza Vcc: 🠞 signif. morbidity/mortality, espicially im/m. ptn. including CKD. In U.K. all CKD ptn. incl. in Vcc. programs 🠞signif. decrease in hospitalization & death in ESRD ptn..

(B) HBV. Vcc.: recmmended for ptn appr. ESRD to avoid transmission among ptn.s & between ptn. & staff. Resp. to Vcc. 🠟as s. Cr.& age rise. It’s successful in mild/ moderate CKD & only 37% in HDX. ptn.s who us. require larger dose than é Normal kid. func.. Immune defects🠞🠟 Vcc. resp.: impaired T-helper cell function, occur due to abn. cytokine signaling & 🠟 expression of HLA Class II molecules by Ag-presenting cells in CKD & ESRD.

- Typical HBV. Vcc schedule:  40 ug., repeated in:    1, 2 & 6 m.    

- Seroconversion: occ. when HB.s A.B. is >10 IU 3 m. after last vaccination.

Q.570. How can immune dysfunction affect cancer evolution in uremics?

A. Immune surveillance is an important mechanism for early detection & deletion of potentially cancerous cells. Immune dysf🠝risk of cancer in a 3 way:  👌 

1)   Direct effect of uremic toxins on immune cell function.

      2)   Underlying renal condition.                         

      3)   ttt of underlying renal condition.

 - This only theoretical, Not evidence-based, only mild🠝in Kid. & UT on DX. ptn.

Q.571 What is the suggested relation between cancer incidence and both Iry renal disease and ongoing therapy?   👉

💣 👽 { Calciphylaxis with Arterial Calcification.} 👀

A. I. Cancer & “Iry”R. dis.:

1)   Von Hipple-Lindau disease.: auto. dom. familial cancer [multiple benign & malignant tumors: Kid., adrenals, CNS & pancreas].

2)   Analgesic NephropathyTransitional cell carcinoma.

3)   Balkan Np. Transitional cell carcinoma.

     II. Cancer & ttt. of R. dis.:

1)   Cph: 🠝 incid. of neoplasia (cancer U.B.), which may appear decades later.

2)   Im/m. é CKD & ESRD: 🠝 risk of cancer.

3)   R.Tx.: certain cancers: more common: non-melanoma “skin” cancer, Post Tx. lmphoprolifertive diso. Risk of neoplasia is linked to reg. used, é mTORs e.g. rapamycin:  Antiproliferative effect & 🠟 risk of neoplasia.

Q.572. What are the treatment options in patients with Calcific Uremic Arteriopathy?  👉

💣  👽  { Calciphylaxis with Arterial Calcification.}  👀

A. I. Cancer & “Iry”R. disease:

A. Treatment options for Calcific Uremic Arteriopathy (CUA) (Calciphylaxis):

(1) Reduction of pro-calcifying factors:

      Intensified: daily HDX., switch fr. P.D. to HDX., Low Ca Dzt.

      Avoid vit. D & Ca supplements, Ca-free Po4 binders, bisphosphonate (cautiously é adynamic bone dis.).

      Pec.(Parathyroidectomy): in severe hyperpara, or use of Cinacalcet - Etelcalcitide.

(2) Improving the status of calcification inhibitors:

Halt vit. K. antagonists (Warfarin).

Aggressive ttt. of infections or other pro-inflmm. stimuli to incr. fetuin-A level (-ve Ac. phase reactant).

Experimental:

o   Vit. K2 high dose.

o   Fetuin-A (by FFP, or Pph.)

(3) Prevention or reversal of Ca-phosphate precipitation:

   Administration of sodium thiosulfate.

(4) Supportive measures:

·         Avoid local tissue trauma by atraumatic wound care é gentle debridement of necrotic tissues & avoid s.c. injections.

·        Improve O2 supply by Hyperbaric therapy.

·        Anticoagulation. (Heparin, LMWH).

·        Adequate pain management.

·        Adequate infection control…

                                                        

Q.573. What are the causes of intradialytic hemolysis?

A. Intradialytic hemolysis:

     I.        Incorrect osmolarity of dialysate.

   II.        Microangiopathy: Drug-induced: e.g Quinine Sulfate.

 III.        Glucose-6-Po4 def.: Exacerbated by oxidants (e.g Quinine Sulfate.).

  IV.        Reductive dge: Formaldehyde (also may activate cold agglutinins).

    V.        Cell membrane fragility:

      Insufficient DX.

      Zinc def.

  VI.        Thermal dge:

  Overheated Dzt. (> 47 °C ).

  Underheated Dzt: (<35°C): anti-N Cold agglutinins activation (formaldehyde).

VII.        Oxidative dge: Methemoglobulinemia:

1.   Chloramines,

2.   Copper.

3.   Nitrate/Nitrites.

4.    Drugs (e.g. Quinie So4).

VIII.        Interference with RBCs metabolism:

1) Copper: affects cellular thiols.

2) Aluminum: affects iron uptake.

3) Formaldehyde: inhibits glycolysis.

4) Hypophosphatemia:2,3-diphosphoglycerate def.

  IX.        Traumatic fragmentation:

(1) Dialyzer roller pump.

(2) Single-needle DX.

(3) Excessive suction arterial access site.

(4) High blood flow thr. a small needle.  

(5) Kinked DX cath./tubing.

(6) RT atrial subclavian cath.

Q.574. What are the causes of HDX-associated seizures?

A. “HDX-associated seizures”:

     I.        Uremic encaphaloopathy.

   II.        Hyperensive encaphaloopathy.

 III.        DX. disequilibrium syndrome.

  IV.        Focal neurologic disease:

1)   Atheroemolism.

2)   Intracranial hge.

3)   Thrombotic microangiopathy.

    V.        Cerebral anoxia due to sustained hypotension:

1)   Hge.

2)   Sepsis.

3)   Cardiac arrhythmia.

4)   Hypersensitivity reaction.

  VI.        Metabolic:

(1)       Hypoglycemia.

(2)       Hypocalcemia.

(3)       Hypomagnesemia.

(4)       Hypernatremia: Hyperosmolarity.

(5)       Severe acid-base disturbances.

VII.        Drugs:

(1) Dialytic removal of anticonvulsats.

(2) Erythropoiesis-stimulating drugs.

(3) Epileptogenic drugs: [Theophylline, Penicillin, Meperidine (its toxic metabolite: normepredine)].

VIII.        Other toxins:

1. Alcohol withdrawal
2. Aluminum intoxication.

Q.575. Describe the evolution of MIA syndrome?   👵👵

A. Malnutrition, Inflammation & Atherosclerosis synd. describes wasting as part of an inflmm. state ass. é CVS dis. It's not responsive to  dietary intake. MIA explains the CVS risk é failing kidney. The evolution of athero. is an inflmmation process, é evidence that CRP enhances this process. CKD ptn have  levels of CRP & other pro-inflmm. cytokines incl. IL-6. The low s. albumin seen in MIA reflects ongoing inflammation & effect of cytokines on GIT, “rather” poor nutritional intake.