Renal

Acute prostatitis This is acute inflammation of the prostate, which usually occurs in infection   Causes Young adults – Chlamydia trachomatis, Neisseria gonorrhoeae Older Adults – E. coli   Symptoms Dysuria, urinary frequency, and suprapubic pain Can cause urinary retention leading to pain and haematospermia Systemic symptoms, e.g., fevers   Key tests DRE gives tender prostate and secretions reveal bacteria   Management Antibiotics e.g. levofloxacin (Quinolone) or Trimethoprim   Benign prostatic hyperplasia (BPH) This refers to hyperplasia of the prostate which occurs with age and is common. It does not increase the risk of cancer, as it is the central

Epididymo-orchitis This is inflammation of the epididymis (and the testes)   Causes Bacteria, e.g., chlamydia, gonorrhea, E. coli Viruses, e.g., mumps (in teenage males) Drugs e.g., amiodarone Symptoms Acute onset tender swelling (confined to epididymis) Dysuria, sweats, fever   Management Treat the underlying cause, e.g., antibiotics if due to an STI   Testicular torsion This refers to twisting of the spermatic cord, usually in adolescents It can cut off the blood supply to the testes resulting in ischaemia   Symptoms Acute onset testicular pain Absence of the cremasteric reflex Abdominal pain, nausea and vomiting Prehn’s sign seen (where raising the

Polycystic kidney disease This is a genetic condition which leads to the development of multiple cysts on the kidneys. It exists as both autosomal dominant and recessive forms:   Autosomal dominant This occurs due to a mutation in the genes PKD1 (Chr 16), or PKD2 (Chr 4) Symptoms Clinically silent initially but gives symptoms in early adulthood  Hypertension (due to renin release), hematuria, cyst infection and kidney failure   Associations Liver cysts (most common extra-renal manifestation) Berry aneurysms in the brain Cardiovascular abnormalities (mitral valve prolapse, valve issues, aortic dissection)   Key tests Abdominal ultrasound is used to detect cysts

Renal Cell Carcinoma (RCC) This refers to a malignant proliferation of kidney cells. It can be sporadic which is associated with increased age, but it is also seen in young children (genetic causes). The most common form is a clear cell carcinoma as the cells look clear on histology   Symptoms Triad of painless hematuria, loin mass and lumbar pain Systemic symptoms e.g., weight loss, fever Paraneoplastic syndromes – due to hormone release, e.g., ACTH, renin, PrPTH Can cause a left-sided varicocele as the tumour may compress the left renal vein   Key tests Ultrasound and CT scan show a

Renal Stones (Nephrolithiasis) This is the presence of a stone which can get lodged somewhere in the urinary tract. It usually in one of the 3 natural points of constriction – pelviureteric junction (PUJ), pelvic brim or vesicoureteric junction (VUJ). There are different types of stones Types of Kidney Stones Risk Factors Dehydration – this increases ion concentration of the urine Recurrent UTIs and foreign bodies which stagnate flow, e.g., stents/catheters Diet – may cause hypercalcaemia and certain foods also increase oxalate levels Underlying metabolic conditions (e.g., hyperparathyroidism)   Symptoms Writhing (colicky) pain which travels from “loin” to groin with

Definition & classification Urinary tract infections (UTIs) refer to an infection of any part of the urinary system from kidney to the urethra. UTIs are generally defined as the presence of characteristic symptoms (e.g. dysuria, frequency) and significant bacteriuria (presence of bacteria in urine). Significant bacteriuria is defined as > 105 colony forming units (CFU)/ml. In the absence of symptoms, this level of bacteriuria is termed asymptomatic bacteriuria. UTIs can be further categorised depending on the location of infection (e.g. upper or lower) or the presence of co-morbidities (e.g. complicated or uncomplicated). Upper UTI: infection of the kidney (pyelonephritis) Lower UTI: infection of the bladder (cystitis) and

Overview Tubulointerstitial nephritis refers to a primary insult to the renal tubules and interstitium. Tubulointerstitial nephritis (TIN) refers to inflammation of the renal tubules and interstitium that is most commonly the result of a hypersensitivity reaction to a medication (e.g. penicillin). This leads to acute inflammation with or without acute kidney injury (AKI). Tubulointerstitial nephritis may be acute or chronic: Acute TIN: develops over days or months. Majority of cases (~85%) due to drugs or infections. May cause AKI to variable severity. Chronic TIN: develops over years. Continued tubulointerstitial insults lead to chronic inflammation and eventually fibrosis with decline in renal function. Most often

Overview Nephrotic syndrome is broadly defined as a triad of heavy proteinuria > 3.5 g/day, hypoalbuminaemia, and oedema. The nephrotic syndrome describes a very classic presentation of glomerular disease that is characterised by a triad of: ‘Nephrotic-range’ proteinuria (> 3.5 g/day) Hypoalbuminaemia (< 35 g/L) Oedema (e.g. peripheral, periorbital) In addition, hyperlipidaemia, increased risk of venous/arterial thrombosis and higher risk of infection is typical of the syndrome. This is because of loss of important proteins (e.g. immunoglobulins, albumin) through the glomeruli. Nephrotic syndrome is one of the hallmarks of glomerular disease. For more general information see our notes on Glomerular disease. Aetiology The cause of

Overview Nephritic syndrome is classically described as the presence of haematuria, variable proteinuria, renal impairment, and hypertension. Nephritic syndrome is also known as glomerulonephritis or simply ‘nephritis’. It describes the presence of an inflammatory process within the glomeruli. The nephritic syndrome describes a very classic presentation of glomerular disease that is characterised by Haematuria Variable proteinuria (may be nephrotic range) Renal impairment Hypertension Glomerulonephritis is a more encompassing term than nephritic syndrome because it reflects the variable clinical presentation of glomerular inflammation. Some patients may have minimal haematuria and proteinuria whereas others develop rapidly progressive renal impairment. Aetiology The cause of nephritic syndrome is

Overview Microscopic polyangiitis (MPA) is a small vessel vasculitis. Microscopic polyangiitis (MPA) is one of the anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitides (AAV) that can present with rapidly progressive renal impairment and other systemic manifestations. In the UK, the incidence is estimated at 2 cases per 100,000 people. It is more common among older Caucasians with an equal sex distribution. ANCA associated vasculitis AAV is an umbrella term for three conditions: Microscopic polyangiitis (MPA) Granulomatosis with polyangiitis (GPA): previously known as Wegener’s granulomatosis Eosinophilic granulomatosis with polyangiitis (EGPA): previously known as Churg-Strauss syndrome These conditions are all small vessel vasculitides that

Overview IgA nephropathy is the most common primary chronic glomerular disease worldwide. It commonly presents with macroscopic haematuria or asymptomatically with microscopic haematuria, proteinuria +/- hypertension picked up incidentally or during investigation for renal impairment. The condition remains a leading caused of chronic kidney disease and renal failure. The diagnosis can be confirmed with a renal biopsy. There is no targeted therapy but angiotensin-converting enzyme (ACE) inhibitors or angiotensin-II receptor blockers (ARB) may be used for proteinuria and hypertension. In those with ongoing severe disease immunosuppressive therapies may be considered. Epidemiology IgA nephropathy predominantly affects children and young adults. Though the disease occurs at

Overview Granulomatosis with polyangiitis (GPA) is a small vessel vasculitis. Granulomatosis with polyangiitis (GPA) is one of the anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitides (AAV) that can present with rapidly progressive renal impairment and other systemic manifestations. In the UK, the incidence is estimated at 10.2 cases per 1,000,000 people. It is slightly more common in men (1.5:1 male to female ratio) and typically presents in middle-age (35-55 years old). ANCA associated vasculitis AAV is an umbrella term for three conditions: Microscopic polyangiitis (MPA) Granulomatosis with polyangiitis (GPA): previously known as Wegener’s granulomatosis Eosinophilic granulomatosis with polyangiitis (EGPA): previously known as

Overview The ‘glomerulopathies’ are a constellation of diseases characterised by injury to renal glomeruli. Glomerular disease (also known as ‘glomerulonephritides’ or ‘glomerulopathies’) refers to a group of conditions that cause damage to the renal glomeruli. The glomeruli represent the site of filtration (i.e. where blood is filtered) within the kidneys. Glomerular diseases are an important cause of both acute kidney injury (AKI) and chronic kidney disease (CKD). Glomerular diseases are traditionally difficult to learn. This is because of confusing terminology that combines clinical and histopathological terms, the wide variety of clinical presentations and significant overlap between conditions. Two commonly discussed clinical manifestations

Overview Chronic kidney disease (CKD) can be defined by the presence of kidney damage or reduced kidney function for three or more months. Reduced kidney function is suggested by a reduction in the glomerular filtration rate (GFR) or by evidence of kidney damage which can be characterised by the presence of one or more of the following pathological markers: Albuminuria (e.g. albumin:creatinine ratio > 3 mg/mmol or > 30 mg/g) Urinary sediment abnormalities (e.g. white cell or red cell casts) Radiological abnormalities (e.g. polycystic kidneys) Pathological abnormalities (e.g. seen on renal biopsy) History of kidney transplantation CKD is a common condition with a progressive nature. As CKD progresses

Overview Anti-glomerular basement membrane (Anti-GBM) disease is a rare small-vessel vasculitis. Anti-glomerular basement membrane (Anti-GBM) disease is a small vessel vasculitis with an annual incidence of one case per million population. It is characterised by the formation of anti-GBM antibodies that are directed against collagen in the kidneys and lungs. This can lead to life-threatening glomerulonephritis and/or pulmonary haemorrhage. Anti-GBM disease is a relatively new term that encompasses the clinical spectrum of both renal and pulmonary manifestations. The condition is associated with two older terms named after Ernest Goodpasture, who initially discovered the condition in 1919: Goodpasture syndrome: refers to clinically

Overview Alport’s syndrome is a rare hereditary nephropathy occurring due to mutations to genes encoding type IV collagen. Alport’s may demonstrate different inheritance patterns though it is most commonly X-linked due to mutations of COL4A5 on the X chromosome. The disease affects the glomerular basement membrane (GBM) leading to nephritis. Other features may include sensorineural hearing loss and ocular defects. Genetics Alport’s may arise from a number of mutations to genes responsible for type IV collagen. It may occur due to mutations to alpha-3, alpha-4 and alpha-5 chains of type IV collagen. Type IV collagen is important to basement membranes and mutations lead to

Overview Autosomal dominant polycystic kidney disease is a common genetic disorder characterised by multiple renal cysts. Autosomal dominant polycystic kidney disease (ADPKD) is due to inheritance of the abnormal genes PKD1 or PKD2 that is thought to occur in around 1 in 1000 live births. The disease is characterised by development of multiple renal cyst and progressive renal impairment, which leads to end-stage renal disease (ESRD) in around 50% of patients by 60 years of age. It accounts for up to 10% of patients with ESRD. ADPKD is generally a condition of adults and rarely presents in childhood. The estimated median age of developing ESRD is in 6th

Overview Acute kidney injury (AKI) is generally defined as a sudden decline in renal function over hours or days. AKI is a common medical condition affecting up to 15% of emergency hospital admissions and the mortality associated with severe AKI can be up to 30-40%. A decline in renal function can lead to dysregulation of fluid balance, acid-base homeostasis and electrolytes. AKI has largely replaced the term ‘acute renal failure’. This change in nomenclature reflects the significance that small decrements in renal function do not lead to overt renal failure, but do have a clinical impact on morbidity and mortality. Classification