Absolute:
1) Severe fluid overload with CCF
2) Severe hyperkalemia unresponsive to medical Rx or with ECG changes
3) Severe hyponeatrmia
4) Server metabloic acidosis requiring > 2 doses of NaHCO3 (2mEq/kg/dose)
5) Uraemia
6) Fluid restriction curtailling ample nutrition

Relative:
1) Anuria
2) High urea and creatinine values alone are not indications

METHOD
Materials:
1) Pertioneal dialysis tubing, trocar and cannula
2) Yellow intracath #14 gauge needle – 12 –24 inches long
3) Cut sown set with narrow blade
4) 2/0 silk on a straight needle
5) peritoneal dialysis fluid 1.5% dianeal (warm the fluid by placing in container of warm water
6) Lignocaine, Iodine, alcohol, mask and sterile gloves

Method: A
1) Consent form to be signed
2) Cross match 1 unit blood
3) Check PT, PTT platelets beforehand
4) Insert urethral catheter to empty bladder
5) Cleanse abdomen with Iodine and alcohol
6) Set up dialysis bags and attach to tubing (fluid should be tepid– not hot and not cold)
7) Determine, before dialysis starts, the volume to be run in and mark out on bag (See Figure 1).
The markings are not exactly in the same position on all bags, so this method is only an
approximation. If more accurate measurement is needed, a Biuretrol must be attached to the
dialysis bag
8 ) Fill tubing with fluid
9) If the abdomen is not tense with ascites, by infusing dialysis fluid until adequate tension is
present one reduces the risk of damaging internal structures eg aorta, inferior vena cava and
bowel. Proceed to step B
10) If the abdomen is already tense with ascites, proceed to step C

B

The procedure is as follows:
1) Remove guide wired from intracath
2) Set up tubing to dialysis fluid
3) Local anaesthetic to skin – superficial and deep at area of proposed intracath insertion
Direct the needle of the intracath downwards gently but firmly
When you feel the “pop” thread the tubing and withdraw the needle around it
Push tubing in as far as it will go – do not press deeply with the needle
4) Run in 30-50 cc/kg of dialysis fluid – sufficient to make abdomen tense
5) Withdraw intracath
6) Proceed to insertion of peritoneal dialysis catheter

C
Insertion of the peritoneal dialysis cannula:
1) Site of catheter – approximately 2 -3 cm inferior to the umbilicus and in the midline
2) Make a small incision at this point with the pointed end of the blade to include skin and subcutaneous
tissues – just big enough for catheter
Figure 1 – Dialysis bags and volume markings
85
3) Hold peritoneal dialysis catheter – with pointed trocar inside. Hand on top of catheter pushing
downwards firmly
4) When you feel the catheter enter the peritoneal cavity (a pop), remove the trocar (pointed internal
metal rod) and thread cannula (plastic part around the trocar) into peritoneal cavity quickly aiming the
cannula to the right or left iliac fossa (R preferably). Push in as far as it will go
5) Connect cannula (dialysis catheter ) to “elbow” and thus the remainder of tubing (already primed with
fluid)
6) Run out fluid from cavity into tubing – should run as a steady stream
7) Pour in expected exchange volume
a) 40-60cc/kg infants and small children
b) 30-40cc/kg older children
Limiting factors – abdominal discomfort, peritoneal leaks
If fluid runs in and out quickly after 3 rapid exchanges – without dwells – put purse string suture
around cannula – tie tightly, fasten securely at the level of the skin then tie 3-4 knots up the side of the
catheter with the same uncut suture

DIALYSIS
Cycles: Usually best clearance with 30 minute cycles :
• In over 5 minutes
• Dwell over 20 minutes
• Drain over 5 minutes
• Tepid fluid
Clearance: Urea > K > Cl > Na > Cr > PO4 > uric acid > HCO3 > Ca > Mg
Dianeal composition: Na 132 K 0 Ca 3.25 Mg 1.3 Cl 101.75 Lactate 35 mmol/l
Rate of water removal (assuming adequate drainage) depends on [glucose] in dialysis fluid
• 1.5% dianeal (1.5% glucose) usually adequate, but may increase to 2.5% or 4.25% if inadequat fluid
removal. If there is no pre-mixed 2.5 % or 4.25% dianeal, they can be prepared as follows
• to make 2.5% from 1.5% – add 40cc of D 50 W / 2 liters of fluid of 1.5% dianeal
• to make 4.25% from 1.5% – remove 110 cc fluid from 2 litre bag of 1.55 dianeal. Add 110 cc of
D50W to bag

ADDITIVES
1) KCl 6 mEq / 2 liters added when serum K <4.0mEq/l
- may be increased in increments of 2-4 mEq/2l bag depending on serum K
2) No antibiotics prophylatically
3) Heparin 1000 units /2 litres of dialysis fluid in all bags to minimize formation of fibrin strands

PERITONITIS
Initial broad spectrum cover for peritonitis.

Empiric therapies:
Intraperitoneal –
1) Cloxacillin 200mg/ 2litres + Gentamycin 10 mg /2 litres (regime used at UHWI with success despite
potential for inactivation when aminoglycosides mixed with penicillins) – Staph is commonest
pathogen for peritonitis here
2) Cefotaxime – 500mg/2 litres
Adjust when sensitivities available

Taken from “ Consensus guidelines for the treatment of peritonitis in pediatric patients receiving peritoneal dialysis” – Peritoneal Dialysis International Vol. 20: 610 – 624

PRECAUTIONS
• Daily peritoneal fluid: c/s, gram stain, cell count. > 100 WBC / ml and > 50% neutrophils suggests
peritonits. – start Rx as soon as sample taken for culture. Fluid is aspirated from the porthole (rubber
bung in tube in the dialysis line near patient entry) with a 25 gauge needle attached to a sterile syringe.
Clean the porthole with Iodine and wrap with Iodine soaked gauze for 10 minutes prior to inserting the
needle, in order to avoid iatrogenic peritonitis.*
• Nurse is asked to call if problems arise (see below)

PROBLEM SOLUTION

Change PD catheter if unable to get good drainage or inflow despite the above measures. Always flush the
tubing with about 20 –50 cc of fluid as catheter is being withdrawn to minimize possibility of omentum
coming up in the catheter as it is being removed. Discontinue dialysis when urine output has improved
sufficiently that the original indications for dialysis are unlikely to recur off dialysis (not just when the lab
results are normal on dialysis

Source- Manual of Nephrology for DM

References:
1) ISPD guidelines / recommendations. Consensus guidelines for the treatment of peritonitis in pediatric
patients receiving peritoneal dialysis. Warady, Schaefer et al. Peritoneal Dialysis International 2000.
20:610 – 624.
2) Paediatric Nephrology (1997) 1: 183 – 194 (for drug dose adjustments)
3) Pediatric Nephrology 15th Edition (1999) Barratt and Vernier Chapter 69 (1125 – 1126)

It is characterized by rapid deterioration of renal functions over days to weeks.

MANAGEMENT of RPGN-

We have elaborated “The regimen used by the Glomerular Disease Collaborative Network at the University of North Carolina at Chapel Hill”

•  Glomerular Disease Collaborative Network at the University of North Carolina at Chapel Hill Regimen is as follows:

  • Administer Methylprednisolone at 7 mg/kg/day IV (not to exceed 1 g) for 3 days,
  • Followed by oral prednisone at 1 mg/kg/d (not to exceed 80 mg) for 3 weeks,
  • Then oral prednisone at 2 mg/kg every other day (not to exceed 120 mg) for 3 months.
  • This dose is decreased by 25% every 4 weeks until the patient stops taking prednisone.

  Therapy for ANCA-associated disease ( Wegener granulomatosis and PAN) consists of a combination of corticosteroids and cyclophosphamide. Treatment with steroids alone results in a 3-fold increase in the risk of relapse compared to combination therapy.

  • Administer cyclophosphamide either intravenously or orally. Intravenous therapy is initially administered at a dose of 0.5 g/m², and the oral dose is 2 mg/kg. Both are adjusted according to a 2-week leukocyte nadir count (goal 3000-4000/µL). The maximum intravenous dose is 1 g/m².
  • Oral and intravenous cyclophosphamide appears to be equally efficacious. However, this remains an area of controversy, particularly in the case of Wegener granulomatosis, for which some advocate oral therapy.

  
• In Europe, azathioprine substitutues cyclophosphamide after a 3-month induction period. Azathioprine is administered at 2 mg/kg orally in a single daily dose. This is continued for 6-12 months.
• Methotrexate has been substituted for cyclophosphamide in the initial treatment of Wegener granulomatosis for mild disease and has been used for treatment after initial induction therapy with cyclophosphamide in more severe disease.
• Plasmapheresis may be a beneficial addition to therapy for patients who present with severe renal failure (serum creatinine >6 mg/dL) or those who progress despite treatment.
• Other medications have been used in an attempt to attain a remission, such as intravenous immunoglobulin, antithymocyte antibody, and humanized monoclonal antibody to CD4 and CD25. None of these therapies has been well studied. They appear in the literature as case reports.
  The only predictor of renal survival is the serum creatinine value at the time of diagnosis. Therefore, a high index of suspicion is imperative to establish the diagnosis quickly and to institute treatment as soon as possible. Renal failure requiring dialysis is not a contraindication to treatment. Many patients can be removed from Dialysis for an extended period (18 mo to 2 y).
  Resources-
  Medscape via
  
  
  Falk RJ, Hogan S, Carey TS, et al. Clinical course of anti-neutrophil cytoplasmic autoantibody-associated glomerulonephritis and systemic vasculitis. The Glomerular Disease Collaborative Network. Ann Intern Med. Nov 1 1990;113(9):656-63.
  Nachman PH, Hogan SL, Jennette JC, et al. Treatment response and relapse in antineutrophil cytoplasmic autoantibody-associated microscopic polyangiitis and glomerulonephritis. J Am Soc Nephrol. Jan 1996;7(1):33-9.

Korotkoff sounds:

When the cuff pressure is great enough to close the artery during part of the arterial pressure cycle, a sound then is heard with each pulsation. These sounds are called Korotkoff sounds believed to be caused mainly by blood jetting through the partly occluded vessel. The jet causes turbulence in the vessel beyond the cuff, and this sets up the vibrations heard through the stethoscope.

As long as the pressure in the cuff is higher than the systolic blood pressure of the patient, blood doesn’t jet through the completely occluded artery, hence no sound is heard. If the pressure is dropped to a level equal to that of the patient’s systolic blood pressure, the first Korotkoff sound will be heard. As the pressure is further gradually lowered down, following korotkoff sounds are heard:

Phase 1 (K1): Clear tapping sounds representing systolic pressure
Phase 2 (K2): Softer tones
Phase 3 (K3): Louder once again
Phase 4 (K4): Muffled Tones sounds representing diastolic pressure
Phase 5 (K5): Tones cease

Auscultatory Gap:

An auscultatory gap also called as silent gap is the interval of pressure where korotkoff sounds indicating true systolic pressure fade away and reappear at a lower pressure point during the manual measurement of blood pressure by auscultatory method. The auscultory gap happens when the first Korotkoff sound fades out for about 20-50 mmHg only to return. It can result in following erroneous blood pressure reading:

1. Underestimation of systolic blood pressure
2. Overestimation of diastolic blood pressure

Example:

The patient’s actual systolic pressure is 200 with a gap from 170 to 140 and a diastolic of 110. You inflate the cuff to 170 and hear nothing until the manometer reaches 140, which you presume is the systolic pressure. Also if you, inflate the cuff to 200, you may read 170 as the diastolic pressure which is the beginning of auscultatory gap.

When recording a blood pressure with an auscultatory gap, always list your complete findings. eg. BP 200/110 with the auscultatory gap from 170 to 140.

Auscultatory gap has been found to occur due to venous pooling of blood. The auscultatory gap is most likely to appear in the obese arm, especially if the physician pumps up the cuff slowly and traps a great deal of blood in the arm’s venous compartment. Another way to trap blood is to pump the cuff 2nd time immediately after 1st determination, without allowing 1-2 minutes for the trapped blood to escape.

Auscultatory gap in Hypertension

An auscultatory gap is common in elderly hypertensive patients. It occurs in some hypertensive patients only. Auscultatory gaps are related to carotid atherosclerosis and to increased arterial stiffness in hypertensive patients, independent of age.

Types:

3 types of auscultatory gaps, have been identified by using wideband external pulse recording.

1. G1: occurs with cuff pressure just below systolic and is characterized by the presence of K1 and K2 with intermittent disappearance of K2. G1 gaps are related to a phasic decrease of arterial (systolic) pressure.
2. G2: are related to a phasic increase of arterial (diastolic) pressure, occur when cuff pressure is just above diastolic, and are characterized by the presence of K1, K2, and K3 with intermittent disappearance of K2.
3. G3: occurs with cuff pressure between systolic and diastolic and are characterized by an underdeveloped or blunted K2 signal.

Mechanism:

• The mechanism of origin of auscultatory gap has not been understood clearly.
• Cavallani recently showed that the early loss of audible sound during cuff deflation is associated with blunted high frequency K2 signals associated with korotkoff sound (detected by wideband external pulse recording) likely related to the altered physical properties of a stiffer arterial wall.

Precautions:

1. Determining systolic blood pressure by palpatory method before recording the blood pressure with auscultatory method.
2. Inflating the blood pressure cuff to 20-40 mmHg higher than the pressure required to occlude the brachial pulse.

Initiator of the disease process by:

1. Antibody mediated injury: immune complex deposition or cytotoxic antibodies
2. T-cell mediated immune injury: non-immune complex deposition mechanism

Secondary immunopathogenic mechanism:

Role of mediators of the disease:

A) Cells:

• Neutrophils and monocytes
• Macrophages, T lymphocytes and NK cells
• Platelets
• Resident glomerular cells (Mesagnial cells)

B) Soluble mediators:

• Complement components
• Eicosanoids, NO, angiotensin and endothelin
• Cytokines: IL-1 and TNF
• Chemokines: MCP-1, RANTES, TGF-B
• Coagulation system

Antibody Mediated Injury

Include:

1. Membranous glomerulonephritis
2. IgA nephropathy
3. Membranoproliferative glomerulonephritis
4. Postinfectious glomerulonephritis
5. Anti-glomerular basement membrane disease

Immune complexes activates complement pathway through classic pathway.

A) In-situ immune complex deposition

1. Fixed intrinsic tissue (Glomerular) antigens:

Mechanism: Circulating antibodies form immune complex against the normal glomerular components

• Glomerular basement mebrane antigens : NC1 domain of collagen type IV antigen (anti-GBM disease)
  • Immunofluorescence: Linear pattern immune-complex deposition
• Podocyte antigens: Heymann antigen (membranous glomerulonephritis)
  • Immunofluorescence: Granular pattern immune-complex deposition
• Mesangial antigens
• Others

2. Planted (Deposited) antigens

Mechanisms: Non-glomerular antigens are deposited in GBM from the circulation firstly and then the circulating antibodies form immune-complex.

Immunofluorescence: Granular pattern immune-complex deposition

• Exogenous antigens (infectious agents, drugs)
• Endogenous antigens (DNA, nuclear proteins, immunoglobulins, immune complexes, IgA)

Factors influencing antigen trapping are: size, charge, molecular configuration and carbohydrate content of antigens.

B) Circulating immune complex deposition

Immunofluorescence: Granular pattern immune-complex deposition

Mechanism: Type III hypersensitivity initiated by antigen-antibody complex formed in the circulation.

• Exogenous antigens (infectious products)
• Endogenous antigens (DNA, tumor antigens)

Localisation of complexes and Factors enhancing it:

Primary immune complex deposition in one site is often accompanied by deposition of lesser amounts in other sites. The factors influencing the localisation complexes are: molecular charge of complexes, size, avidity (strength of bond between antigen and antibody), blood flow, etc.

1. Subendothelial (between capillary endothelium and GBM):

• Charge: Highly anionic complexes excluded from GBM
• Size: Intermediate
• Avidity: High

2. Intramembranous (within GBM):

• Charge: Represents the transitional phase in which complexes migrate from subendothelial position to subepithelial
• Blood flow: Increased

3. Subepithelial (between epithelial cells and GBM):

• Charge: Highly cationic complexes
• Size: Smallest (pass freely through the glomerulus without being trapped)
• Avidity: Low

4. Mesangial (within mesangium):

• Charge: Neutral charge
• Size: Large
• Blood flow: Decreased

C) Cytotoxic antibodies

Cell mediated immune injury

Mechanism: Non-immune complex deposition glomerulonephritis

This may occur through regulation of B-cell differentiation and antibody production or by local cell-mediated immunity i.e. delayed-type hypersensitivity reaction. The later is initiated by CD4+ cells by activating monocytes/macrophages which produces cytokines: IL12, IL2, INF-γ and TNF-a which are powerful inflammatory mediators causing injury. CD8+ cells acts by their cytotoxic ability.

Includes:

1. Minimal Change Disease (Lipoid necrosis)
2. Focal segmental glomerulosclerosis

Activation of Alternative Complement Pathway

Alternative pathway of complement pathway is activated by complex polysaccharides.

Role of Complement: C₃ & C₅ are chemoattractant for leukocytes, neutrophils in particular which causes damage by releasing proteolytic enzymes and by generating reactive oxygen metabolites. Terminal complement components C₅b-9, membrane attack complex (MAC) causes injury by basement membrane lysis.

Non-immunologic Mechanism

Hemodynamic and physical forces that cause intraglomerular HTN and abnormal stress and strain on the vascular wall.

Relationship of Physiologic role of glomerular components with consequences of glomerular injury

A) Endothelial cells:

Physiologic function –> Consequence of injury –> Related Disease

1. Maintain glomerular perfusion –> Vasoconstriction –> Acute renal failure
2. Prevent leukocyte adhesion –> Leukocyte infiltration –> Focal/diffuse GN
3. Prevent platelet aggregation –> Intravascular microthrombi –> Thrombotic microangiopathies

B) Mesangial cells:

• Physiologic function: Control glomerular filtration
• Consequence of injury: Proliferation and increased matrix
• Related Disease: Membranoproliferative GN

C) Visceral epithelial cells (Podocytes):

• Physiologic function: Prevent plasma protein filtration
• Consequence of injury: Proteinuria
• Related disease: Minimal change disease, Focal Segemntal Glomerulosclerosis

D) Glomerular Basement Membrane (GBM):

• Physiologic function: Prevents plasma protein filtration
• Consequence of injury: Proteinuria
• Related disease: Membranous GN

E) Parietal epithelial cells:

• Physiologic function: Maintain Bowman’s space
• Consequence of injury: Crescent formation
• Related disease: Rapidly Progressive Glomerulonephritis (RPGN)

Summary:

a) Non-immune mechanisms are involved in Diabetic nephropathy

b) Detected anibody deposition pattern: Granular except in Anti-GBM Nephritis (Linear)

c) Sites of Immune complex or Antigen Deposition:

• Subepithelial: Poststreptococcal Glomerulonephritis
• Epimembranous: Membranous Glomerulonephritis
• Subendothelial: SLE, Type I Membranoproliferative Glomerulonephritis (MPGN)
• Mesangial: IgA Nephropathy
• Basement membrane: Type II MPGN