Causes of Renal Impairment in a Patient with Rheumatoid Arthritis

This patient has longstanding rheumatoid arthritis treated with gold and is currently experiencing an exacerbation of her symptoms. The presence of renal impairment with mild proteinuria and haematuria suggests a potential underlying cause. Amyloidosis is a common complication in patients with longstanding rheumatoid arthritis, which presents with proteinuria often in the nephrotic range. Gold nephropathy is another potential cause of proteinuria, but haematuria is rare. Interstitial nephritis may also account for the changes seen in this patient, especially since she is taking diclofenac, which is known to cause renal impairment.

Non-steroidal anti-inflammatory drugs (NSAIDs) are another potential cause of renal impairment, which can lead to a reversible reduction in the glomerular filtration rate, acute tubular necrosis, acute interstitial nephritis, renal papillary necrosis, and chronic tubulointerstitial nephritis. Myeloma is also a possibility, but there is no evidence of this in the patient’s presentation. Vasculitis is a rare cause of renal impairment in rheumatoid arthritis, which presents with proteinuria, microscopic haematuria, and renal impairment. However, since this cause is less common than interstitial nephritis associated with NSAIDs, it is not the most likely explanation in this case.

In summary, there are several potential causes of renal impairment in a patient with rheumatoid arthritis, including amyloidosis, gold nephropathy, interstitial nephritis, NSAIDs, myeloma, and vasculitis. A thorough evaluation is necessary to determine the underlying cause and appropriate treatment.

Diabetes insipidus is a medical condition that can be caused by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary gland (cranial DI) or an insensitivity to ADH (nephrogenic DI). Cranial DI can be caused by various factors such as head injury, pituitary surgery, and infiltrative diseases like sarcoidosis. On the other hand, nephrogenic DI can be caused by genetic factors, electrolyte imbalances, and certain medications like lithium and demeclocycline. The common symptoms of DI are excessive urination and thirst. Diagnosis is made through a water deprivation test and checking the osmolality of the urine. Treatment options include thiazides and a low salt/protein diet for nephrogenic DI, while central DI can be treated with desmopressin.

Complications Associated with ADPKD

Hypertension is a common early finding in patients with ADPKD, and it should be managed aggressively with standard antihypertensive medications. Intracerebral aneurysms are found in up to 2% of patients with ADPKD, which may lead to subarachnoid or intracerebral haemorrhage, the most severe of the complications associated with ADPKD. Mitral valve prolapse is also found in 20% of patients with ADPKD. Additionally, there is an increased incidence of aneurysms and arterial dissections in patients with ADPKD. However, aortic stenosis is not associated with ADPKD.

It is important to be aware of the potential complications associated with ADPKD, as early detection and management can prevent severe consequences. Hypertension should be closely monitored and treated promptly to prevent further damage to the kidneys and other organs. Patients with ADPKD should also be screened for intracerebral aneurysms and mitral valve prolapse, as these conditions can lead to serious health issues. Finally, an increased incidence of aneurysms and arterial dissections should be considered when evaluating patients with ADPKD.

Understanding Cholesterol Embolism and Differential Diagnosis

Cholesterol embolism is a condition commonly seen in patients with existing arterial disease who have undergone arterial manipulation. Patients may present with a peripheral purpuric rash and dusky lower limbs, and associated laboratory tests include eosinophilia, worsening kidney disease, raised erythrocyte sedimentation rate (ESR), and low levels of complement. Unfortunately, there is no specific treatment shown to be of benefit.

When considering a differential diagnosis, contrast nephropathy can occur after a contrast load in patients with renal impairment, but it would not account for the eosinophilia in this case. Acute vasculitis is a systemic illness that presents with a palpable purpura that occurs in crops, along with other associated symptoms such as fever, weight loss, fatigue, and joint pains. Renal artery thrombosis can cause renal impairment due to complete occlusion of the renal artery from thromboemboli, atherosclerosis, or fibromuscular disease, but it would not cause an eosinophilia. Renal vein thrombosis, on the other hand, occurs most commonly in patients with nephrotic syndrome with heavy proteinuria, hypoalbuminemia, hypercholesterolemia, and peripheral edema due to a hypercoagulable state.

In summary, understanding the presentation and associated laboratory tests of cholesterol embolism and considering differential diagnoses can aid in proper diagnosis and management of patients.

The patient’s underlying diagnosis is still unknown, but it is evident that she is suffering from acute kidney injury. The reason for her seizure is also unclear, but given the normal CT head, uraemia is a possible cause. The renal team has decided to perform dialysis on the patient because they suspect symptomatic uraemia, which could be the reason for her seizure. While an elevated urea level alone is not an indication for dialysis, a urea level of >25 mmol/l, along with concomitant symptoms, could be considered for dialysis to prevent uraemic symptoms from progressing. Similarly, a creatinine level of >1000 µmol/l is indicative of severe renal impairment but not an indication for dialysis. Dialysis would only be considered if the patient’s potassium level is >6.5 mmol/l or if the pH level is <7.1. A pH level of 7.34 is not severe enough to warrant dialysis. Before resorting to dialysis, attempts would be made to medically treat the patient's potassium levels. The NICE guidelines for acute kidney injury (AKI) identify several risk factors, including emergency surgery, CKD, diabetes, and use of nephrotoxic drugs. Diagnostic criteria for AKI include a rise in creatinine, a fall in urine output, or a fall in eGFR. The KDIGO criteria are used to stage AKI based on the severity of the creatinine increase or reduction in urine output. Referral to a nephrologist is recommended for certain cases, such as stage 3 AKI, inadequate response to treatment, or complications of AKI.

Microscopic Polyangiitis and ANCA-Associated Vasculitis

Microscopic polyangiitis is a type of ANCA-associated vasculitis that is characterized by a positive ANCA and either a strongly positive anti-PR3 (cANCA) or anti-MPO (pANCA) antibody. The MPO antibody is typically associated with microscopic polyangiitis, while the PR3 antibody is linked to Granulomatosis with polyangiitis. ANCA-associated vasculitis is a group of autoimmune diseases that cause inflammation of blood vessels, leading to damage in various organs. In microscopic polyangiitis, the inflammation affects small blood vessels in the kidneys, lungs, and skin. Early diagnosis and treatment are crucial to prevent organ damage and improve outcomes.

Diagnosis of Autosomal Dominant Polycystic Kidney Disease

Autosomal dominant polycystic kidney disease (ADPKD) is a genetic disorder that can be diagnosed through renal ultrasound screening. This test has a sensitivity of 100% for PKD1, but false negatives may occur in individuals under the age of 20. If cysts are not detected, the ultrasound should be repeated every five years until the age of 30. Some experts recommend starting screening at a younger age to allow for early diagnosis and management of hypertension, which can slow disease progression.

Abdominal CT is also sensitive for detecting cysts, but its high radiation dose makes it unsuitable for widespread use as a screening test. Genetic testing is only used in specific circumstances, such as when a definite diagnosis is required in a young patient or for potential living donors. However, this method can only identify around 70% of known mutations, and linkage analysis requires the availability of sufficient family members.

Intravenous urography is no longer used in the diagnosis of ADPKD, and magnetic resonance angiography is typically only recommended for patients with a diagnosis of ADPKD who have symptoms of an intracranial aneurysm, a previous ICA, a high-risk job should intracranial haemorrhage occur, or an affected family member with an ICA. Regular screening and early detection are crucial for managing ADPKD and preventing complications.

Management and Prevention of Renal Stones

Renal stones, also known as kidney stones, can cause severe pain and discomfort. The British Association of Urological Surgeons (BAUS) has published guidelines on the management of acute ureteric/renal colic. Initial management includes the use of NSAIDs as the analgesia of choice for renal colic, with caution taken when prescribing certain NSAIDs due to increased risk of cardiovascular events. Alpha-adrenergic blockers are no longer routinely recommended, but may be beneficial for patients amenable to conservative management. Initial investigations include urine dipstick and culture, serum creatinine and electrolytes, FBC/CRP, and calcium/urate levels. Non-contrast CT KUB is now recommended as the first-line imaging for all patients, with ultrasound having a limited role.

Most renal stones measuring less than 5 mm in maximum diameter will pass spontaneously within 4 weeks. However, more intensive and urgent treatment is indicated in the presence of ureteral obstruction, renal developmental abnormality, and previous renal transplant. Treatment options include lithotripsy, nephrolithotomy, ureteroscopy, and open surgery. Shockwave lithotripsy involves generating a shock wave externally to the patient, while ureteroscopy involves passing a ureteroscope retrograde through the ureter and into the renal pelvis. Percutaneous nephrolithotomy involves gaining access to the renal collecting system and performing intracorporeal lithotripsy or stone fragmentation. The preferred treatment option depends on the size and complexity of the stone.

Prevention of renal stones involves lifestyle modifications such as high fluid intake, low animal protein and salt diet, and thiazide diuretics to increase distal tubular calcium resorption. Calcium stones may also be due to hypercalciuria, which can be managed with thiazide diuretics. Oxalate stones can be managed with cholestyramine and pyridoxine, while uric acid stones can be managed with allopurinol and urinary alkalinization with oral bicarbonate.

Management of Severe Malaria with Acute Kidney Injury

Severe malaria with associated acute kidney injury (AKI) requires urgent treatment to prevent high mortality rates. Renal impairment is common in adults with severe falciparum infection and is caused by disease in glomeruli, tubules, and the interstitial region. Clinical manifestations of malaria-associated AKI include oligo-anuria, severe metabolic acidosis, and a hypercatabolic state. The mainstay of treatment involves administering appropriate antimalarial drugs parenterally, such as intravenous artesunate, alongside supportive measures like IV fluids and dialysis to treat AKI. Hyperkalaemia should also be addressed with IV calcium. While a repeat blood film can confirm the diagnosis, initiating treatment is the priority. Blood transfusion is not necessary unless there is co-existent symptomatic anaemia. Acute dialysis may be required if there are complications like pulmonary oedema, life-threatening hyperkalaemia, or metabolic acidosis resistant to medical treatment. However, the preferred method would be haemodialysis, not peritoneal dialysis. Urine microscopy and culture are not the next most important step in management as the patient has not passed urine due to AKI.

Pseudohyponatraemia in Nephrotic Syndrome: Understanding the Mechanism and Diagnosis

Pseudohyponatraemia is a condition where the measured sodium level in the blood appears low, but the actual sodium concentration is normal. In patients with nephrotic syndrome, pseudohyponatraemia can occur due to hyperlipidaemia. The excess lipids in the blood exclude electrolytes from the plasma volume, leading to a spurious low sodium result. However, the plasma osmolality remains normal. It is important to diagnose pseudohyponatraemia as no treatment is required.

Spot urinary sodium can be useful in differentiating the cause of acute kidney disease. A low urinary sodium suggests a pre-renal cause.
Plasma antidiuretic hormone level would be normal and would not help in discerning the cause of hyponatraemia.
The Short synacthen test would be normal in this case, but abnormal in Addison’s disease.
Urine osmolality would be high in cases of pre-renal kidney disease, but not helpful in this case.