The patient underwent a bowel resection due to UC, which puts them at risk for developing oxalate stones. The stone is visible on imaging, ruling out urate and xanthine stones. Staghorn calculi, which involve the renal pelvis and at least 2 calyces, are not present as the stone is located in the ureter.

Renal stones come in different types, each with its own appearance on x-ray. Calcium oxalate stones are the most common, accounting for 40% of cases, and appear opaque on x-ray. Mixed calcium oxalate/phosphate stones make up 25% of cases and also appear opaque. Triple phosphate stones, which are composed of ammonium magnesium phosphate, account for 10% of cases and have an opaque appearance. Calcium phosphate stones also appear opaque and make up 10% of cases. Urate stones, which are made of uric acid, are radiolucent and account for 5-10% of cases. Cystine stones are rare, accounting for only 1% of cases, and have a semi-opaque, ‘ground-glass’ appearance. Xanthine stones are the rarest, accounting for less than 1% of cases, and are also radiolucent. Stag-horn calculi are large stones that involve the renal pelvis and extend into at least 2 calyces. They develop in alkaline urine and are composed of struvite (ammonium magnesium phosphate, triple phosphate). Ureaplasma urealyticum and Proteus infections predispose to their formation.

Aminoglycoside related renal damage primarily affects the proximal tubule, where the drug molecules bind to anion phospholipids in the plasma membrane of proximal tubular cells. This leads to their uptake and transportation by lysosomes to the Golgi body, where they act as a mitochondrial poison. Gentamicin specifically impacts cells in the proximal tubule, while cisplatin is toxic for distal tubular epithelial cells. The collecting duct is not affected by aminoglycosides, but water absorption is regulated by aquaporin-2 expression, which can be influenced by bile salts. The loop of Henle is not the primary site of toxicity for aminoglycosides, as it mainly reabsorbs water and ions. Vascular endothelial cells are not damaged by gentamicin, but renoprotective agents like ACE inhibitors, ARBs, and SGLT-2 inhibitors can improve microvascular function and inhibit efferent arteriolar vasoconstriction.

A young woman who has developed acute kidney injury and visual problems is likely suffering from TINU syndrome, which is characterized by tubulointerstitial nephritis and uveitis. This condition is commonly seen in young women and is accompanied by symptoms such as fever, weight loss, and uveitis. Urinalysis typically shows the presence of pyuria and proteinuria. Treatment with steroids is usually effective in resolving the kidney injury. Other conditions such as scleroderma and nephrocalcinosis may cause similar symptoms but are less likely to present acutely in this manner.

Acute interstitial nephritis is a condition that is responsible for a quarter of all drug-induced acute kidney injuries. The most common cause of this condition is drugs, particularly antibiotics such as penicillin and rifampicin, as well as NSAIDs, allopurinol, and furosemide. Systemic diseases like SLE, sarcoidosis, and Sjögren’s syndrome, as well as infections like Hanta virus and staphylococci, can also cause acute interstitial nephritis. The histology of this condition shows marked interstitial oedema and interstitial infiltrate in the connective tissue between renal tubules. Symptoms of acute interstitial nephritis include fever, rash, arthralgia, eosinophilia, mild renal impairment, and hypertension. Sterile pyuria and white cell casts are common findings in investigations.

Tubulointerstitial nephritis with uveitis (TINU) is a condition that typically affects young females. Symptoms of TINU include fever, weight loss, and painful, red eyes. Urinalysis is positive for leukocytes and protein.

Haemodialysis for Acid-Base and Electrolyte Disturbance Correction

Haemodialysis is an effective treatment for correcting acid-base and electrolyte disturbances in patients. This process involves the use of a machine to filter the blood and remove excess waste products and fluids from the body. During haemodialysis, the patient’s blood is passed through a dialysis machine, which removes excess fluids and waste products, including excess electrolytes and acids. This helps to restore the balance of electrolytes and acids in the body, which can be disrupted in patients with kidney failure or other conditions.

Haemodialysis is a highly effective treatment for correcting acid-base and electrolyte disturbances, and it is often used in patients with kidney failure or other conditions that affect the body’s ability to regulate these levels. By removing excess fluids and waste products from the body, haemodialysis helps to restore the balance of electrolytes and acids, which can improve overall health and wellbeing. With regular haemodialysis treatments, patients can maintain healthy levels of electrolytes and acids, which can help to prevent complications and improve their quality of life.

Thiazide diuretics can reduce calcium excretion and the formation of renal stones in patients with hypercalciuria. This patient has a history of two episodes of renal colic caused by renal stones, as evidenced by calcification on abdominal x-ray. The composition of the stones is likely to contain a significant amount of calcium, which is commonly found in calcium phosphate or calcium oxalate stones. Thiazide diuretics are effective in preventing hypercalciuria-related stones, such as calcium phosphate stones, while potassium citrate may be useful for calcium oxalate stones. Allopurinol is recommended for uric acid stones, which are typically not visible on plain x-ray imaging.

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 ureteric 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 intra corporeal 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.

This woman is diagnosed with stage IV chronic kidney disease and has an estimated glomerular filtration rate (eGFR) of less than 30ml/min.

The initial treatment for hypertension in this population is still an ACE inhibitor or angiotensin receptor blocker.

However, chronic kidney disease is a unique case where the standard NICE hypertension algorithm does not apply to second-line management. Diuretics are utilized to aid in salt excretion and reduce hypertension. Loop diuretics, such as furosemide, are the preferred option for patients with an eGFR of less than 30ml/min.

Chronic kidney disease (CKD) patients often require more than two drugs to manage hypertension. The first-line treatment is ACE inhibitors, which are especially effective in proteinuric renal disease like diabetic nephropathy. However, these drugs can reduce filtration pressure, leading to a slight decrease in glomerular filtration pressure (GFR) and an increase in creatinine. NICE guidelines state that a decrease in eGFR of up to 25% or a rise in creatinine of up to 30% is acceptable, but any increase should prompt careful monitoring and exclusion of other causes. If the rise is greater than this, it may indicate underlying renovascular disease.

Furosemide is a useful anti-hypertensive drug for CKD patients, particularly when the GFR falls below 45 ml/min*. It also helps to lower serum potassium levels. However, high doses are usually required, and if the patient is at risk of dehydration (e.g. due to gastroenteritis), the drug should be temporarily stopped. The NKF K/DOQI guidelines suggest a lower cut-off of less than 30 ml/min.

IgA nephropathy is a condition that presents with haematuria post-respiratory tract infection and is more common in males in their second and third decades. The disease is characterized by histological findings on renal biopsy. Management includes controlling hypertension with ACE inhibitors and using corticosteroids. In cases of crescenteric nephritis, intravenous pulsed corticosteroids are employed with the addition of cyclophosphamide. A low-protein diet may reduce proteinuria, but it is not used alone to control symptoms. Calcium channel antagonists are not preferred over ACE inhibitors as they may even increase proteinuria. Ciclosporin may be considered later on for disease control, but early on, cyclophosphamide is added to the steroid regimen. ACE inhibitors are the preferred agents to control blood pressure and proteinuria. Fortunately, progression to end-stage renal disease is uncommon in this condition, and renal transplantation carries a high chance of success.

In most cases, non-contrast CT scans of the abdomen can detect renal tract calculi. However, there are rare instances where a radiolucent stone on CT KUB can result in a missed diagnosis.

Certain medications such as furosemide, acetazolamide, and allopurinol can increase the risk of developing calcium oxalate, calcium phosphate, and uric acid stones respectively. Calcium stones can be seen on both plain x-ray and CT scans, while uric acid stones can only be detected with CT. However, if urine is supersaturated with indinavir, it can lead to the formation of pure indinavir stones that are not visible on either plain x-ray or CT scans.

The recommended initial treatment for indinavir stones is hydration and pain relief, but discontinuing the medication may be necessary temporarily or permanently.

It is important to note that tenofovir does not increase the risk of renal stone formation.

Renal stones come in different types, each with its own appearance on x-ray. Calcium oxalate stones are the most common, accounting for 40% of cases, and appear opaque on x-ray. Mixed calcium oxalate/phosphate stones make up 25% of cases and also appear opaque. Triple phosphate stones, which are composed of ammonium magnesium phosphate, account for 10% of cases and have an opaque appearance. Calcium phosphate stones also appear opaque and make up 10% of cases. Urate stones, which are made of uric acid, are radiolucent and account for 5-10% of cases. Cystine stones are rare, accounting for only 1% of cases, and have a semi-opaque, ‘ground-glass’ appearance. Xanthine stones are the rarest, accounting for less than 1% of cases, and are also radiolucent. Stag-horn calculi are large stones that involve the renal pelvis and extend into at least 2 calyces. They develop in alkaline urine and are composed of struvite (ammonium magnesium phosphate, triple phosphate). Ureaplasma urealyticum and Proteus infections predispose to their formation.

When a person experiences symptoms of excessive thirst and drinking (polydipsia), the possible causes include diabetes insipidus, psychogenic polydipsia, and diabetes mellitus (which has been ruled out in this case). To diagnose diabetes insipidus, a water deprivation test is conducted to differentiate between nephrogenic diabetes insipidus (when the kidneys are not sensitive enough to ADH release by the posterior pituitary), cranial diabetes insipidus (when there is a lack of ADH release from the posterior pituitary, but the kidneys respond to exogenous ADH when administered), and psychogenic polydipsia (when the water deprivation test results are normal). In this case, the patient’s serum osmolality increases as expected during the water deprivation test, but the urine does not concentrate much, and there is minimal response by the kidneys to DDAVP. This indicates nephrogenic diabetes insipidus, as psychogenic polydipsia would show concentrated urine earlier in the test with high urine osmolalities, and in cranial diabetes insipidus, the kidneys would respond more to DDAVP by concentrating the urine.

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.

Patients with type one diabetes who are approaching end stage renal failure should be evaluated for the possibility of receiving a combined pancreas and renal transplant. However, any decisions regarding renal replacement therapy should be made with a multidisciplinary approach and tailored to the patient’s lifestyle and preferences. While a pancreas and renal transplant can replace renal function and treat the underlying cause of dysfunction, it also requires lifelong immunosuppression. Haemodialysis, which is typically performed at a local dialysis centre or at home three times a week, and peritoneal dialysis, which allows for more mobility but carries a risk of peritonitis, are other options. As renal replacement therapy is a complex decision that requires extensive workup, it should be considered early in the presence of progressive renal disease. It is important to note that a pancreas transplant alone may address diabetes but not renal function, which could complicate options in the future if renal function continues to deteriorate.

The HLA system, also known as the major histocompatibility complex (MHC), is located on chromosome 6 and is responsible for human leucocyte antigens. Class 1 antigens include A, B, and C, while class 2 antigens include DP, DQ, and DR. When matching for a renal transplant, the importance of HLA antigens is ranked as DR > B > A.

Graft survival rates for renal transplants are high, with a 90% survival rate at one year and a 60% survival rate at ten years for cadaveric transplants. Living-donor transplants have even higher survival rates, with a 95% survival rate at one year and a 70% survival rate at ten years. However, postoperative problems can occur, such as acute tubular necrosis of the graft, vascular thrombosis, urine leakage, and urinary tract infections.

Hyperacute rejection can occur within minutes to hours after a transplant and is caused by pre-existing antibodies against ABO or HLA antigens. This type of rejection is an example of a type II hypersensitivity reaction and leads to widespread thrombosis of graft vessels, resulting in ischemia and necrosis of the transplanted organ. Unfortunately, there is no treatment available for hyperacute rejection, and the graft must be removed.

Acute graft failure, which occurs within six months of a transplant, is usually due to mismatched HLA and is caused by cell-mediated cytotoxic T cells. This type of failure is usually asymptomatic and is detected by a rising creatinine, pyuria, and proteinuria. Other causes of acute graft failure include cytomegalovirus infection, but it may be reversible with steroids and immunosuppressants.

Chronic graft failure, which occurs after six months of a transplant, is caused by both antibody and cell-mediated mechanisms that lead to fibrosis of the transplanted kidney, known as chronic allograft nephropathy. The recurrence of the original renal disease, such as MCGN, IgA, or FSGS, can also cause chronic graft failure.