Creatinine and Calcium Homeostasis in CKD 3 Patients

In patients with CKD 3, elevated creatinine levels indicate a decline in kidney function. However, interpreting creatinine levels can be challenging without considering factors such as body habitus and muscle mass. To determine the severity of CKD 3, an eGFR calculation can be performed, which typically results in a value of 30-59 ml/min/1.73m2.

Patients with CKD 3 may experience multiple abnormalities in calcium homeostasis. While plasma concentrations of calcium and phosphate are usually normal at this stage, subtle changes may occur as CKD3 progresses towards CKD 4. For example, reduced hydroxylation of vitamin D by the kidney enzyme 1-alpha hydroxylase can lead to a slight increase in PTH levels.

Vitamin D insufficiency is common in CKD3 patients and can be caused by various risk factors such as old age, immobility, institutionalization, and darker skin color. While suboptimal levels of vitamin D may contribute to calcium homeostasis abnormalities, it is not the only factor to consider in CKD3 management.

Diagnosis and Management of HIV Nephropathy

HIV infection is a high possibility in a patient with risk factors and presenting with emaciation, oral ulcers, and lymphopenia. A CD4 count and HIV serological testing should be done urgently. HIV nephropathy is a common complication, with focal and segmental glomerulosclerosis being the most common pathological diagnosis. Other variants include membranoproliferative nephropathy, diffuse proliferative glomerulonephritis, minimal change disease, and IgA nephropathy. Treatment involves ACE inhibitors and antiretroviral therapy, with dialysis being necessary in end-stage disease. Renal biopsy is required to confirm the diagnosis, but HIV testing should be performed first. Serum IgA levels are elevated in IgA nephropathy, while serum complement levels and anti-nuclear factor are needed in SLE-associated nephropathy or other connective tissue diseases or vasculitis. However, the lack of systemic symptoms points away from these diagnoses.

Plasma Exchange and its Side Effects

Plasma exchange is a medical procedure that involves taking blood from a patient, separating the cells and large proteins from the plasma and smaller proteins, and replacing the plasma with either donated fresh-frozen plasma or human albumin solution. This process removes low molecular weight proteins such as antibodies, but it also has a number of side effects. These side effects are partly due to the removal of other components such as clotting factors, but they are also due to the blood products and anticoagulants used.

To address these complications, more specific methods of antibody removal have been developed, such as immunoabsorption. This method uses a column of beads coated in specific antigen, which separates the plasma and passes it over the column. Antigen-specific antibodies bind to the column, and antibody-free plasma can then be returned to the patient. This method is better for the patient because they do not lose clotting factors and avoid exposure to blood products.

Common side effects of plasma exchange include hypocalcaemia, which is a decrease in plasma ionised calcium due to the citrate anticoagulants used for replacement fluids such as human albumin solution and fresh frozen plasma. Bleeding can also occur due to the loss of clotting factors in the exchange, and transfusion with any blood products can lead to allergic reactions. Infection is also a risk due to the loss of protective immunoglobulins along with the autoantibodies, so it is important to monitor immunoglobulin levels during treatment.

New Onset Diabetes After Transplantation (NODAT)

New onset diabetes after transplantation (NODAT) is a condition that is becoming increasingly common among transplant recipients. It is estimated that between 5-20% of recipients develop NODAT within the first year after transplantation, and up to 30% in the longer term. The use of prednisolone is often associated with NODAT, especially in patients who had impaired glucose tolerance before the transplant. However, calcineurin inhibitors such as ciclosporin and tacrolimus are also known to increase the risk of NODAT. The risk of NODAT with ciclosporin is around 5%, while it can be as high as 20% with tacrolimus. Sirolimus, another immunosuppressive drug, is also believed to be diabetogenic, with similar rates to ciclosporin. It is worth noting that cyclophosphamide is not used in transplantation immunotherapy, while azathioprine and mycophenolate mofetil are not associated with NODAT.

Hyperphosphataemia and Itching in End Stage Renal Failure Patients

Patients with end stage renal failure often experience hyperphosphataemia, which is caused by the loss of renal control over calcium/phosphate balance. This occurs because the kidneys are no longer able to excrete phosphate and produce activated vitamin D. As a result, calcium levels decrease, leading to secondary hyperparathyroidism, which maintains calcium levels but at the expense of raised phosphate levels. Hyperphosphataemia can cause itching and dermatitis, making it important to restrict dietary phosphate intake and use phosphate binders taken with meals to prevent phosphate absorption.

While anaemia is common in dialysis patients, it does not typically cause itching. Polycythaemia, which can occur in patients with polycystic kidney disease due to excessive erythropoietin production, can cause itching, but this is unlikely to be the cause of itching in this patient with end stage renal failure. Hypovolaemia may cause dry skin, but it is unlikely to cause an itchy rash. Hypophosphataemia is also extremely unlikely in renal patients and does not tend to cause itching.

Causes of Haematuria

Haematuria, or blood in the urine, can be caused by various factors. Measles is not one of them. However, conditions such as meatal ulcer and urinary tract infection can lead to haematuria. Additionally, an advanced Wilms’ tumour can also cause this symptom. Another cause of haematuria is Schistosomiasis, which is a parasitic infection caused by Schistosoma haematobium. In this case, the blood in the urine is due to bladder involvement. It is important to identify the underlying cause of haematuria in order to provide appropriate treatment and prevent further complications.

Patients with end stage kidney disease have poor iron absorption and lack endogenous erythropoietin, making parenteral iron replacement and erythropoietin the best management. Anaemia is common in these patients due to poor oral iron absorption and GI blood loss. Acute packed red cell transfusion is extreme and renal transplant may be an option, but the patient’s haemoglobin can be modified with increased IV iron and epo doses. Oral iron tablets are poorly absorbed and tolerated.

The only teratogenic drug must be stopped prior to conception, while the risks of other medications must be balanced against the risks to the mother. The combination of tacrolimus, azathioprine, and steroids is considered the safest. If the patient is taking mycophenolate or sirolimus, they should be changed to azathioprine or a calcineurin inhibitor, respectively. Bisoprolol is generally safe in pregnancy, but if the patient becomes pregnant, they may need to switch to methyldopa or labetalol as alternative antihypertensives and receive closer monitoring in a joint clinic. Transplant patients should wait at least 12 months after surgery before trying to conceive and should be stable for at least six months without complications before doing so.

Acute Tubular Necrosis and Tubulo-Interstitial Nephritis

Acute tubular necrosis (ATN) is a condition that occurs when the kidneys experience prolonged hypotension and poor perfusion, leading to the death of tubular epithelium. This can result in complete anuria, which is the absence of urine output. While a blocked catheter is unlikely, a bladder scan should be performed to rule it out. ATN can also be caused by nephrotoxins and sepsis. The condition usually recovers over a few days to weeks, but if the patient has underlying renal disease, the recovery may be partial, leading to long-term chronic kidney disease (CKD). Therefore, pre-renal failure should be corrected as quickly as possible to prevent irreversible damage.

Tubulo-interstitial nephritis (TIN) is a histological diagnosis that occurs when the tubules and interstitium of the kidney become inflamed due to drugs or infections. This can lead to the release of cytokines and infiltration by acute inflammatory cells, particularly lymphocytes and eosinophils. If the causative agent is removed, TIN can resolve. However, if it persists, tubular atrophy and interstitial fibrosis may occur, leading to end-stage renal failure. Oral steroids can be used to dampen the inflammation and prevent fibrosis, but they need to be started early in the disease course.

In summary, ATN and TIN are two conditions that can cause kidney damage and lead to CKD or end-stage renal failure. While ATN is caused by prolonged hypotension and poor perfusion, TIN is caused by drugs or infections. Early intervention is crucial to prevent irreversible damage and promote recovery.

Treatment Options for ANCA Vasculitis

ANCA vasculitis is a condition that causes inflammation of blood vessels, leading to organ damage. To treat this condition, induction agents such as cyclophosphamide and rituximab are used in severe or very active cases. Cyclophosphamide is a chemotherapy drug that causes DNA crosslinking, leading to apoptosis of rapidly dividing cells, including lymphocytes. On the other hand, rituximab is a monoclonal antibody that targets CD20, causing profound B cell depletion.

For maintenance or steroid-sparing effects, azathioprine and mycophenolate mofetil are commonly used. However, they take three to four weeks to have their maximal effect, making them unsuitable for severe or very active cases. Ciclosporin, a calcineurin inhibitor, is not widely used in the treatment of ANCA vasculitis, despite its use in transplantation to block IL-2 production and proliferation signals to T cells.

In summary, the treatment options for ANCA vasculitis depend on the severity of the disease. Induction agents such as cyclophosphamide and rituximab are used in severe or very active cases, while maintenance agents like azathioprine and mycophenolate mofetil are used for mild cases. Ciclosporin is not commonly used in the treatment of ANCA vasculitis.