Test: Hemodialysis & Kidney Transplantation - NEET PG MCQ

Indications for emergency dialysis can be summarised using the acronym AEIOU:

• Acidosis, particularly if severe (pH ≤ 7.2 and resistant to HCO₃ or unable to administer HCO₃ due to fluid overload) or symptomatic (e.g., arrhythmias).
• Electrolyte imbalances, especially potassium when accompanied by EKG changes. Temporary measures may include Ca, D₅₀, insulin, bicarbonate, and kayexalate.
• Ingestions, particularly those leading to renal failure such as salicylates or ethylene glycol.
• Overload, specifically volume overload resulting in pulmonary oedema. Temporary management can involve nitrates and high doses of Lasix (160-200 mg IV) - administer slowly to prevent ototoxicity.
• Uremia, which may present as confusion, pericarditis, seizures, or platelet dysfunction with significant bleeding, as well as intractable nausea and vomiting.

When considering the initiation of dialysis in chronic kidney disease (CKD), it should commence whenever the glomerular filtration rate (GFR) falls below 15 ml/min and there is one or more of the following conditions:

• Symptoms or signs of uraemia.
• Inability to manage hydration status or blood pressure.
• Progressive decline in nutritional status.

In any scenario, dialysis ought to begin before the GFR drops to 6 ml/min/1.73 m², even if optimal pre-dialysis care has been administered and no symptoms are present.

• Gram-positive organisms are typically observed, followed by gram-negative organisms.

• Discomfort and turbid dialysate, frequently accompanied by fever and other systemic symptoms.

• Infections caused by gram-negative rods are less prevalent.
• Fungal and mycobacterial infections may occur in specific patients, particularly following antibacterial treatment.

• Fistulas boast the highest long-term patency rate among all dialysis access methods.

For the majority of patients with ESRD, around 9 to 12 hours of dialysis are necessary each week, typically split into three equal sessions. Current Goals of Haemodialysis include:

• Urea reduction ratio (the fractional decrease in blood urea nitrogen per haemodialysis session) of >65-70%
• Body water-indexed clearance x time product (KT/V) higher than 1.2 or 1.05

Hypotension is the most prevalent acute complication associated with haemodialysis. Since the adoption of bicarbonate-containing dialysate, the occurrence of dialysis-related hypotension has diminished. Managing hypotension during dialysis involves:

• Stopping ultrafiltration
• Administering 100-250 mL of isotonic saline or 10 mL of 23% saturated hypertonic saline
• Giving salt-poor albumin

In general, for tunneled CDCs, the most suitable veins for central access are:

• right internal jugular (RIJ)
• right external jugular (REJ)
• left internal jugular (LIJ)
• left external jugular (LEJ)

The National Kidney Foundation's Kidney Disease Outcomes Quality Initiative Clinical Practice Guidelines for Haemodialysis Adequacy (K/DOQI Guidelines) recommend avoiding subclavian vein (SCV) catheterisation in patients with end-stage renal disease (ESRD) due to the potential risk of central venous stenosis, which may lead to the complete loss of the entire ipsilateral arm for vascular access.

• A urea reduction ratio (the percentage decrease in blood urea nitrogen per haemodialysis session) of >65-70%.
• A body water-indexed clearance times volume (KT/V) greater than 1.2 or 1.05.

• Halting ultrafiltration.
• Administering 100-250 mL of isotonic saline or 10 mL of 23% saturated hypertonic saline.
• Providing salt-poor albumin.

Haemodialysis can lead to various complications. The following points outline these complications:

• Hypotension: A drop in blood pressure, which can cause dizziness or fainting.
• Bleeding tendency: Increased risk of bleeding due to factors like anticoagulant use.
• Hypertension: High blood pressure that may occur in some patients.

However, peritonitis is not a complication associated with haemodialysis. It is more commonly linked to peritoneal dialysis.

Hypotension is the most prevalent acute complication associated with haemodialysis, especially in individuals with diabetes mellitus. Several factors seem to elevate the likelihood of hypotension, such as:

• excessive ultrafiltration combined with insufficient compensatory vascular filling,
• impaired vasoactive or autonomic responses,
• osmolar shifts,
• overzealous use of antihypertensive medications,
• and diminished cardiac reserve.

Patients with arteriovenous fistulas and grafts may experience high output cardiac failure due to the diversion of blood through the dialysis access; in rare instances, this could require the ligation of the fistula or graft.

Dialysis-related amyloidosis:

• Represents approximately 50% of individuals undergoing haemodialysis for 8-12 years.
• The amyloid protein involved is Aβ₂M-globulin.
• Typically develops in conjunction with chronic haemodialysis, almost never occurring before 5 years of treatment.
• Visceral deposits are infrequent.
• Osteoarticular deposits are prevalent; common symptoms include carpal tunnel syndrome, flexor tenosynovitis, bone cysts, and pathological fractures.
• Systemic manifestations generally appear only after 15 years of haemodialysis and may involve cardiac, gastrointestinal, and renal issues.
• In addition to supportive care, treatment may include the use of high-flux biocompatible polyarylonitrile and polysulfone dialysis membranes, which improve the removal of β₂M proteins.
• Renal transplantation may be an option.

Dialysis is a medical procedure used to remove waste products and excess fluids when the kidneys are not functioning properly. The following are some important conditions that typically require dialysis:

• Persistent Hyperkalaemia: High levels of potassium in the blood can be dangerous and often necessitate dialysis.
• Congestive Cardiac Failure: When the heart cannot pump effectively, dialysis may help alleviate the burden on the heart.
• Pulmonary Oedema: Fluid accumulation in the lungs can be relieved through dialysis.

However, Hyperphosphatemia, which refers to high phosphate levels in the blood, is generally not considered an absolute indication for dialysis. Other treatments are usually available for managing this condition.

Cardiovascular disease is the primary cause of mortality in individuals with ESRD. The rates of cardiovascular death and events are significantly greater in dialysis patients compared to those following transplantation, although both groups experience alarmingly high rates. The exact reason for cardiovascular disease remains uncertain but may be associated with common risk factors, including:

• diabetes mellitus
• hypertension
• atherosclerotic and arteriosclerotic vascular diseases

Other contributing factors may include:

• chronic inflammation
• extensive fluctuations in extracellular volume (particularly with substantial weight gains between dialysis sessions)
• insufficient management of hypertension
• dyslipidemia
• anemia
• dystrophic vascular calcification
• hyperhomocysteinemia
• and possibly changes in cardiovascular dynamics during dialysis treatment.

The uremic environment results in uremic encephalopathy, as urea is capable of crossing the blood-brain barrier. This urea causes irritation to the stomach lining, resulting in persistent nausea and vomiting among these patients.

• Due to the kidneys' inability to eliminate protons, metabolic acidosis develops.
• However, dialysis facilitates the removal of urea, leading to an improvement in the patient’s condition.

Nonetheless, the bone alterations caused by secondary hyperparathyroidism in these individuals result in osteitis cystica fibrosa and Rugger-jersey spine, which cannot be rectified without a kidney transplant or the administration of calcitriol along with calcium supplementation.

Hyperkalemia of 6.5 mEq/dl is not considered life-threatening and requires medical treatment. Only in cases of refractory, life-threatening hyperkalemia is hemodialysis necessary. There are several clinical reasons to commence dialysis in patients with chronic kidney disease (CKD). These include:

• Pericarditis or pleuritis (urgent indication).
• Progressive uremic encephalopathy or neuropathy, characterised by symptoms such as confusion, asterixis, myoclonus, wrist or foot drop, or, in severe instances, seizures (urgent indication).
• A clinically significant bleeding diathesis caused by uremia (urgent indication).
• Persistent metabolic abnormalities resistant to medical treatment; these include hyperkalemia, metabolic acidosis, hypercalcemia, hypocalcemia, and hyperphosphatemia.
• Fluid overload unresponsive to diuretics.
• Hypertension that poorly responds to antihypertensive medications.
• Ongoing nausea and vomiting.
• Signs of malnutrition.

The first five indications above can potentially be acutely life-threatening and should not be permitted to progress before initiating dialysis in patients with known CKD who are receiving medical care. The last two conditions tend to develop more gradually and may also stem from other comorbidities or medication effects. They are equally hazardous.

In individuals undergoing long-term haemodialysis, osteomalacia is linked to the build-up of aluminium in bone. Research has indicated that those on haemodialysis exposed to dialysate with elevated aluminium levels face a heightened risk of developing osteomalacia. Common symptoms may comprise:

• Proximal muscle weakness
• Bone pain
• Multiple non-healing fractures
• Acute or subacute changes in mental status
• Premature osteoporosis

These patients generally exhibit some level of renal disease, with most receiving either haemodialysis or peritoneal dialysis.

The image depicts the rhabditiform larva of Strongyloides stercoralis.

• Choice A is eliminated because it is a dioecious organism associated with parthenogenesis.
• Choice B is dismissed since it is transmitted through skin penetration by larvae.
• Choice C is excluded as Loeffler pneumonia results from ascariasis.

• The risk is highest between 5 and 13 weeks post-transplantation.
• The patient is at risk of graft failure.

CMV infection cannot be identified solely based on clinical symptoms; instead, quantitative nucleic acid testing for CMV using PCR technology is the most appropriate method for diagnosis.

• The virus may be present in urine for months or even years following a recent infection, making urine microscopy or immunofluorescence unreliable for diagnosis.
• IgM anti-CMV is utilised to diagnose recent infections but can yield false positives due to the presence of Rheumatoid factor.
• On the other hand, the IgG anti-CMV antibody has the drawback of taking four weeks to become detectable.

Epidemiologically, P. malariae demonstrates the most definitive incidence of inducing renal parenchymal diseases, such as nephrotic syndrome.

The most common ocular infection after renal transplantation is caused by a virus known as Cytomegalovirus. This virus can lead to serious complications in patients who have undergone kidney transplants due to their weakened immune systems.

• Cytomegalovirus is prevalent among renal transplant patients.
• It can cause vision problems and may lead to blindness if not treated.
• Monitoring for this virus is crucial after transplantation to prevent complications.

Donation after cardiac death
I: Brought in dead
II: unsuccessful Resuscitation
III; Awaiting Cardiac Arrest
IV; Cardiac arrest after Brainstem Death
V: Cardiac arrest In a Hospital patient
Kidneys for transplantation can be used from categories II-V but are commouly used from categories III and IV

The incidence of tumors in patients on immuno-suppressive therapy is 5 - 6 % , or approximately 100 times greater than that in the general population in the same age range. The most common lesions are cancer of the skin and lips and carcinoma in situ of the cervix, as well as lymphomas such as non- Hodgkin's lymphoma. The risks are increased in proportion to the total immunosuppressive load administered and the lime elapsed since transplantation. Surveillance for skin and cervical cancers is necessary.

The life expectancy for a graft from a living donor is around 20 years, while that for a graft from a deceased donor is approximately 14 years.

Selective renal arteriography is conducted in donors to eliminate the possibility of multiple or abnormal renal arteries. This is due to the technical challenges involved in organ removal and the increased ischaemia time of the transplanted kidney. The donor kidney is connected to the recipient's external or internal iliac artery and is situated in the right iliac fossa. Therefore, the recipient renal angiogram referenced in option A is unnecessary. To reduce the risk of early acute rejection, induction therapy is administered using antithymocyte globulin (a polyclonal antibody), which promotes lymphocyte depletion. Additionally, the monoclonal antibody alemtuzumab, which targets the CD52 antigen found on B and T cells, can also be beneficial. Following this, maintenance therapy consists of a triple regimen:

• Prednisolone
• Calcineurin inhibitor: Cyclosporine or tacrolimus
• Antimetabolite: Azathioprine or mycophenolate mofetil

Alternatively, an mTOR inhibitor can replace the last two agents (calcineurin inhibitor and antimetabolites), with sirolimus and everolimus as options. Acute rejection episodes may manifest with fever, swelling, and tenderness around the allograft, although this is infrequently observed. Most acute rejection incidents are characterised by an elevation in serum creatinine levels without a substantial decrease in urine output. The treatment for an acute rejection episode involves administering methylprednisolone for three days. If this proves ineffective, antithymocyte globulin may be utilised.

Recurrence of kidney lesions after transplantation

• Secondary causes of membranoproliferalive (mesangiocapillary) glomerulonephritis (MPGN) (type I) indude infections such as viral hepatitis B or C and systemic diseases. Treatment of these underlying causes may thus reduce the risk of recurrence. Recurrent disease should also be differentiated from de novo MPGN which occurs as part of the histological changes in patients with chronic transplant nephropathy.

• SLE and Goodpasture's syndrome are autoimmune disorders where a continual antibody response attacks the transplanted kidney.
• In diabetic individuals, inadequate sugar control can lead to microvascular damage in the transplanted kidney.

In Minimal Change Glomerulonephritis, the light microscopic changes typically show:

• No abnormality in the structure of the glomeruli.
• However, there may be fusion of foot processes, which are the tiny projections on the cells that line the glomeruli.
• It is important to note that there is usually an absence of Immunoglobulins in the affected areas.
• Additionally, there is typically an absence of complement proteins in the glomeruli.

These findings are crucial for understanding the disease and its effects on kidney function.

• Antibodies can trigger a type of antibody-dependent, yet cell-mediated cytotoxicity by recipient cells that possess receptors for the Fc portion of immunoglobulin.
• Cellular rejection is driven by lymphocytes that react to HLA antigens present in the organ.
• The CD4⁺ lymphocyte reacts to class II (HLA-DR) incompatibility by proliferating and releasing pro-inflammatory cytokines, which enhance the proliferative response of both CD4⁺ and CD8⁺ cells.
• CD8⁺ cytotoxic lymphocyte precursors primarily respond to class I (HLA-A, -B) antigens, maturing into cytotoxic effector cells.
• The cytotoxic effector ('killer') T cells inflict organ damage through direct contact and lysis of donor target cells.

• PRA (Percent Reactive Antibody) indicates the level of HLA antibody present in a patient's serum.
• A patient may possess HLA antibodies due to transfusions, previous transplants, and/or pregnancies.

• Each of these groups contains numerous specific HLA proteins; for instance, there are 59 distinct HLA-A proteins, 118 different HLA-B proteins, and 124 various HLA-DR proteins.

In this case, the boy is experiencing generalized edema and shows signs of albuminuria in his urine tests, along with low serum albumin levels and high fat levels in the blood. Despite a normal appearance in the kidney under light microscopy, the electron microscopy is key to identifying the underlying issue.
The most likely finding in the electron microscopy is:

• Fusion of foot processes of the glomerular epithelial cells.