Renal disease: renal Flashcards

1
Q

How does renal disease often present?

A

Renal disease can present as an incidental finding, symptomatic condition, or as a result of being associated with a systemic disorder.

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2
Q

Name some systemic disorders associated with renal disease.

A

Renal disease can be associated with systemic lupus erythematosus (SLE), sarcoidosis, myeloma, and certain inherited diseases.

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3
Q

What are some indicators of incidental renal disease?

A

Abnormal renal function tests, urinary abnormalities, hypertension, or the presence of a small or dilated kidney on imaging can indicate incidental renal disease.

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4
Q

Why is renal disease often asymptomatic?

A

Renal disease is often asymptomatic because there can be large changes in the glomerular filtration rate (GFR) without a significant increase in creatinine levels, especially in the early stages. Additionally, kidneys have significant excess capacity, with GFR needing to drop below 50% before creatinine levels rise above the normal range. Symptoms related to reduced kidney function are typically uncommon until GFR drops below 15.

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5
Q

What are some commonly measured blood tests used to assess renal function?

A

Commonly measured blood tests used to assess renal function include sodium, potassium, urea, creatinine, bicarbonate, arterial blood gases (pH), and lactate levels.

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6
Q

What is hyperkalemia?

A

Hyperkalemia refers to the elevated levels of potassium in the blood, which can be indicative of renal dysfunction.

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7
Q

What are some urinary abnormalities that can be detected through urinalysis?

A

Urinalysis can detect non-visible blood, protein, glucose, ketones, bilirubin, pH, nitrites, and leucocytes in the urine.

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8
Q

What is proteinuria, and how is it detected?

A

Proteinuria refers to the presence of protein in the urine. It can be detected using a dipstick test to see a list of proteins. Up to 200 mg of protein in a 24-hour urine collection is usually insignificant. Different types of renal pathology are associated with different protein loss.

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9
Q

How can proteinuria be measured without a 24-hour urine collection?

A

Proteinuria can be measured using the protein/creatinine ratio (PCR) or the albumin/creatinine ratio (ACR). The PCR/ACR (mg/mmol) multiplied by 10 is approximately equal to the 24-hour excretion of protein in milligrams (mg/24 hrs).

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10
Q

Why is proteinuria screening important for general practitioners (GPs)?

A

GPs are increasingly required to screen for proteinuria in patients with conditions such as diabetes, chronic kidney disease (CKD), and cardiovascular risk. Screening for proteinuria helps in assessing kidney function and determining appropriate management strategies.

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11
Q

What are the benefits of using the albumin/creatinine ratio (ACR) for proteinuria testing?

A

Albumin testing using the ACR has become the standard assay for proteinuria. It provides a more accurate assessment of albumin excretion and is particularly useful in detecting early stages of kidney damage.

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12
Q

How does proteinuria impact chronic kidney disease (CKD) progression?

A

Proteinuria increases the risk of CKD progression. Protein itself can be nephrotoxic to the tubules, further contributing to kidney damage. If proteinuria is present, more aggressive targets are often set for the treatment of blood pressure to help slow down the progression of CKD.

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13
Q

How does increased proteinuria affect renal function?

A

Increased proteinuria is associated with a faster decline in renal function. Higher levels of protein in the urine indicate greater kidney damage and can be indicative of worsening renal disease.

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14
Q

How can non-visible haematuria be differentiated using urine tests?

A

Non-visible haematuria can be evaluated using urine microscopy to identify red cell casts. The presence of red cell casts indicates glomerular disease. Alternatively, bleeding from the lower renal tract, such as the renal pelvis downwards, can be caused by conditions like tumors, stones, or even bladder catheterization.

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15
Q

How does renal disease often present?

A

Renal disease can present as an incidental finding, meaning it is discovered unexpectedly or manifests with symptoms. Additionally, renal disease can be associated with systemic disorders or inherited diseases that are detected through screening processes.

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16
Q

What are some symptoms of symptomatic renal disease?

A

Symptoms of symptomatic renal disease can include general malaise, “uraemia” symptoms (fatigue, lethargy, confusion, anorexia, nausea, sense of smell and taste changes), nephrotic syndrome (characterized by proteinuria, edema, and hypoalbuminemia), nephritic syndrome (characterized by hematuria, hypertension, and renal impairment), acute kidney injury (acute renal failure), chronic kidney disease, visible hematuria, urinary symptoms (such as increased frequency and dysuria), and pain.

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17
Q

What are some symptoms and signs of uremia?

A

Symptoms of uremia can include fatigue, lethargy, confusion, anorexia, nausea, sense of smell and taste changes, cramps, restless legs, insomnia, and itching. Signs of uremia can include amenorrhea, hiccups, reduced body temperature, weight loss, pericarditis, pleurisy, seizures, and encephalopathy.

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18
Q

What are some signs of renal disease?

A

Signs of renal disease can include peripheral edema (swelling in the extremities), purpura (small purple spots on the skin caused by bleeding), muddy brown urine, foamy urine (resembling cola), and periorbital edema (swelling around the eyes).

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19
Q

What are some causes of renal disease?

A

Some causes of renal disease include pre-renal acute kidney injury (hypovolemia, cardiac failure, hepatorenal syndrome), renal artery occlusion, large/medium vessel vasculitis, small vessel disease (thrombotic microangiopathy, renal atheroembolism, small vessel vasculitis), glomerular disease (anti-GBM disease, lupus nephritis, postinfectious glomerulonephritis, infective endocarditis, membranoproliferative glomerulonephritis, cryoglobulinemia, IgA nephropathy/Henoch-Schönlein purpura), acute tubular injury/necrosis (caused by drugs, aminoglycosides, antiretrovirals, cisplatin, acetaminophen, radiocontrast agents, organic solvents, IV immunoglobulin), acute interstitial nephritis (caused by drugs, infections, systemic diseases), intra-tubular obstruction (cast nephropathy, drugs, crystalluria), and post-renal obstruction (papillary necrosis, tumors, retroperitoneal fibrosis, renal calculi, urinary retention).

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20
Q

What are the key features of the normal glomerulus structure?

A

The key features of the normal glomerulus structure include capillaries with fenestrated epithelium, a basement membrane, a single layer of epithelial cells called podocytes, foot processes of podocytes, and supporting mesangial cells.

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21
Q

What can cause injury to podocytes?

A

Podocyte injury can be caused by various factors, including cytokines (e.g., minimal change disease), increased pressure (e.g., hypertensive glomerulopathy), and immunoglobulin deposition (e.g., IgA nephropathy).

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22
Q

What are the patterns and causes of glomerular disease?

A

The patterns and causes of glomerular disease can vary. The diagnosis of kidney disease is often made based on clinical presentation, but a renal biopsy can provide an accurate diagnosis. Patterns of disease can be observed on light microscopy, electron microscopy, and immunofluorescence for antibodies.

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23
Q

How are diseases of the glomerulus diagnosed?

A

Diseases of the glomerulus are often diagnosed clinically based on specific symptoms and medical history. However, a renal biopsy is often necessary to provide an accurate diagnosis. Light microscopy, electron microscopy, and immunofluorescence for antibodies are used to identify patterns and specific features of glomerular diseases.

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24
Q

What is glomerulonephritis?

A

Description: Glomerulonephritis refers to inflammation in the glomerulus, which is the filtering unit of the kidney.

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25
Q

What is the difference between focal and diffuse glomerulonephritis?

A

Description: Focal glomerulonephritis involves less than 50% of the glomeruli on light microscopy, while diffuse kidney filtering unitre than 50% of the glomeruli.

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26
Q

What is segmental glomerulonephritis?

A

Description: Segmental glomerulonephritis refers to inflammation that involves only a part of the glomerular tuft, usually in a focal manner.

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27
Q

What is membranous glomerulonephritis?

A

Description: Membranous glomerulonephritis is characterized by thickening of the glomerular capillary wall, often with distinctive basement membrane “spikes.” It does not involve inflammation.

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28
Q

What are proliferative changes in the glomeruli?

A

Description: Proliferative glomerulonephritis refers to an increased number of cells in the glomerulus, which can be either proliferating glomerular cells or infiltrating circulating inflammatory cells.

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29
Q

What are some examples of glomerulonephritis?

A

Description: Examples of glomerulonephritis include minimal change disease, membranous glomerulonephritis, and focal proliferative glomerulonephritis. Each has distinct histological findings and characteristics.

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30
Q

What is Type 1 immune disease of the glomerulus?

A

Description: Type 1 immune disease involves immediate hypersensitivity reactions mediated by IgE. However, there is no known renal disease associated with this type of immune response.

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31
Q

What is Type 2 immune disease of the glomerulus?

A

Description: Type 2 immune disease is characterized by antibody-mediated tissue injury. It involves the binding of IgG and IgM antibodies to target cells or matrix components, leading to complement activation and tissue injury at the site. Examples of Type 2 immune diseases of the glomerulus include membranous glomerulonephritis, anti-GBM disease, ANCA-associated glomerulonephritis/polyangiitis, and antibody-mediated graft rejection.

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32
Q

What is Type 3 immune disease of the glomerulus?

A

Description: Type 3 immune disease involves the formation of immune complexes in the circulation, which deposit within the glomerulus and cause tissue injury by recruiting immune mediators. Examples of Type 3 immune diseases of the glomerulus include lupus nephritis, post-infectious glomerulonephritis, glomerulonephritis associated with hepatitis B or C, and cryoglobulinemic glomerulonephritis.

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33
Q

What is Type 4 immune disease of the glomerulus?

A

Description: Type 4 immune disease is T cell-mediated and involves macrophage activation and inflammation. It includes CD8+ T cell-mediated direct cell cytotoxicity. Examples of Type 4 immune diseases of the glomerulus include sarcoidosis and systemic sclerosis-related tubulointerstitial nephritis, as well as acute graft rejection.

34
Q

What is Type 2 immune disease of the glomerulus?

A

Description: Type 2 immune disease is characterized by antibody-mediated tissue injury. It involves the binding of IgG and IgM antibodies to target cells or matrix components, leading to complement activation and tissue injury at the site. Examples of Type 2 immune diseases of the glomerulus include membranous glomerulonephritis, anti-GBM disease, ANCA-associated glomerulonephritis/polyangiitis, and antibody-mediated graft rejection.

35
Q

What is Type 3 immune disease of the glomerulus?

A

Description: Type 3 immune disease involves the formation of antigen-antibody complexes in the circulation, which then deposit within the glomerulus and cause tissue injury due to the recruitment of immune mediators. Examples of Type 3 immune diseases of the glomerulus include lupus nephritis, post-infectious glomerulonephritis, glomerulonephritis associated with hepatitis B or C, and cryoglobulinemic glomerulonephritis.

36
Q

What is Type 4 immune disease of the glomerulus?

A

Description: Type 4 immune disease is T cell-mediated and involves macrophage activation and inflammation. It includes CD8+ T cell-mediated direct cell cytotoxicity. Examples of Type 4 immune diseases of the glomerulus include sarcoidosis and systemic sclerosis-related tubulointerstitial nephritis, as well as acute graft rejection.

37
Q

What is Type 2 immune disease of the glomerulus?

A

Description: Type 2 immune disease is characterized by antibody-mediated tissue injury. It involves the binding of IgG and IgM antibodies to target cells or matrix components, leading to complement activation and tissue injury at the site. Examples of Type 2 immune diseases of the glomerulus include membranous glomerulonephritis, anti-GBM disease, ANCA-associated glomerulonephritis/polyangiitis, and antibody-mediated graft rejection.

38
Q

What is Type 3 immune disease of the glomerulus?

A

Description: Type 3 immune disease involves the formation of antigen-antibody complexes in the circulation, which then deposit within the glomerulus and cause tissue injury due to the recruitment of immune mediators. Examples of Type 3 immune diseases of the glomerulus include lupus nephritis, post-infectious glomerulonephritis, glomerulonephritis associated with hepatitis B or C, and cryoglobulinemic glomerulonephritis.

39
Q

How do antibodies cause damage in immune diseases of the glomerulus?

A

Description: In antibody-mediated immune diseases of the glomerulus, antibodies directly bind to target cells, receptors, or proteins. This binding can lead to complement activation, activation of cell death reactions, and subsequent tissue injury.

40
Q

How does antigen-antibody complex deposition cause tissue injury in the glomerulus?

A

Description: In antigen-antibody complex-mediated immune diseases of the glomerulus, immune complexes form in the circulation elsewhere in the body. These complexes can then become trapped within the glomerulus, triggering inflammation and tissue injury. The effects of this process depend on the specific location of the complex deposition within the glomerulus.

41
Q

What are the histological findings in membranous glomerulonephritis?

A

Description: Membranous glomerulonephritis is characterized by diffuse thickening of the basement membranes in the glomerulus. On immunofluorescence, there are diffuse granular deposits of IgG immunocomplexes along the peripheral glomerular capillary walls.

42
Q

What are the histological findings in diffuse proliferative glomerulonephritis?

A

Description: Diffuse proliferative glomerulonephritis can be associated with a post-streptococcal sore throat. On histology, there is an increased number of cells in the glomerulus, and the capillaries may be occluded by inflammatory cells (indicated by arrows). On immunofluorescence, there are sparse deposits of IgG immunocomplexes along the capillary loops.

43
Q

What are some causes of small vessel disease in the kidneys?

A

Small vessel disease in the kidneys can be caused by various conditions, including thrombotic microangiopathy (characterized by abnormal clot formation in small blood vessels), renal atheroembolism (occlusion of small renal vessels by cholesterol-rich plaques), and small vessel vasculitis (inflammation of small blood vessels).

44
Q

What are some causes of glomerular disease?

A

Glomerular disease can have various causes, including anti-GBM disease (autoimmune disorder leading to inflammation of glomerular basement membrane), lupus nephritis (kidney inflammation associated with systemic lupus erythematosus), postinfectious glomerulonephritis (glomerular inflammation following an infection), infective endocarditis (infection of the heart valves leading to glomerular damage), membranoproliferative glomerulonephritis (thickening of the glomerular capillary walls), cryoglobulinemia (presence of abnormal proteins in the blood leading to glomerular injury), and IgA nephropathy/Henoch-Schönlein purpura (abnormal deposition of IgA immune complexes in the glomeruli).

45
Q

What are some manifestations of small vessel disease in the kidneys?

A

Small vessel disease in the kidneys can manifest as vasculitis (inflammation of the vessels), thrombosis (blockage due to blood clots), atherosclerosis (narrowing of the vessels), hypertension (high blood pressure), and diabetes.

46
Q

What is the histological finding associated with hypertensive nephropathy?

A

Hypertensive nephropathy is characterized by atherosclerosis of the afferent arteriole and glomerulosclerosis with mesangial proliferation.

47
Q

What are the biopsy findings associated with hypertensive nephropathy?

A

Biopsy findings in hypertensive nephropathy include glomerular sclerosis (thickening and scarring of the glomeruli), tubular atrophy (loss of kidney tubules), and arteriosclerosis (thickening and narrowing of the arteries). There are no immune deposits observed on immunohistochemistry (IHC).

48
Q

What are the clinical features of hypertensive nephropathy?

A

Hypertensive nephropathy is more common in African individuals than Caucasians. It is associated with chronic hypertension and is the second most common cause of end-stage renal disease. Clinical features may include haematuria (blood in urine) with variable proteinuria (presence of excess protein in urine).

49
Q

What is the treatment for hypertensive nephropathy?

A

Treatment for hypertensive nephropathy involves using antihypertensive medications, such as ACE inhibitors, to achieve blood pressure control below 130/80 mmHg.

50
Q

What are the histological findings associated with diabetic glomerulonephropathy?

A

In diabetic glomerulonephropathy, the basement membrane of the efferent arteriole and obstruction is thickening. Increased pressure within the glomerulus leads to hyperfiltration. Mesangial cells secrete intracellular matrix, contributing to the expansion of the glomerulus. Over time, there may be the development of nodular glomerulosclerosis.

51
Q

What are the biopsy findings associated with diabetic nephropathy?

A

Diabetic nephropathy is typically diagnosed clinically; biopsies are rarely performed. However, if a biopsy is done, the characteristic finding is nodular glomerulosclerosis, which refers to the presence of nodules in the glomeruli.

52
Q

What are the clinical features of diabetic nephropathy?

A

Diabetic nephropathy is commonly seen in individuals with a median duration of diabetes mellitus (DM) of around 10 years. It is the most common cause of end-stage renal disease (ESRD) worldwide, accounting for 30% of all ESRD cases in patients with DM. There is often a progressive increase in albuminuria (excess protein in the urine) before the onset of overt kidney disease. Diabetic nephropathy can present with nephrotic syndrome and is frequently associated with other microvascular complications of DM, such as retinopathy or neuropathy.

53
Q

What is the management approach for diabetic nephropathy?

A

The management of diabetic nephropathy includes blood pressure control, reduction of proteinuria using ACE inhibitors or similar medications, and optimal control of diabetes itself.

54
Q

What are some examples of renal syndromes?

A

Renal syndromes include nephrotic syndrome (characterized by heavy proteinuria, low serum albumin levels, edema, and hyperlipidemia), nephritic syndrome (characterized by hematuria, proteinuria, hypertension, and mild to moderate renal impairment), acute kidney injury (AKI, sudden decline in kidney function), and chronic kidney disease (CKD, progressive and irreversible loss of kidney function over time).

55
Q

What are the clinical features of nephrotic syndrome?

A

Nephrotic syndrome is characterized by a triad of proteinuria (excess protein in the urine), low levels of albumin (a type of protein) in the blood, and edema (swelling). Additional associated features include high cholesterol levels and a tendency to thrombosis (formation of blood clots).

56
Q

What is the pathophysiology of nephrotic syndrome?

A

The pathophysiology of nephrotic syndrome involves several mechanisms. The kidneys become “leaky,” allowing large molecules like albumin to pass through into the urine. This reduces colloid osmotic pressure in the blood, causing salt and water to leak into the tissues, leading to edema. The activation of the renin-angiotensin system in response to decreased blood volume results in fluid retention. Proteinuria in nephrotic syndrome includes the loss of Antithrombin III, leading to an increased tendency for clotting. There is also increased hepatic protein synthesis, resulting in hyperlipidemia (high levels of lipids, including cholesterol, in the blood).

57
Q

What are the characteristic features of haematuria in renal disorders?

A

Haematuria in renal disorders can present as either microscopic (not visible to the naked eye) or macroscopic (visible) blood in the urine. In some cases, haematuria can appear as “muddy brown” or “Coca Cola” colored urine.

58
Q

What are the characteristic features of nephritic syndrome?

A

Nephritic syndrome is characterized by haematuria, often with the presence of red blood cell casts in the urine. Other features include hypertension (high blood pressure), acute kidney injury, proteinuria (usually less than 3.5 grams per day), and increased risk of venous thromboembolism (blood clot formation).

59
Q

What are the characteristic features of nephrotic syndrome?

A

Nephrotic syndrome is characterized by severe proteinuria (excessive protein loss in the urine, typically exceeding 3.5 grams per day), hypoalbuminemia (low levels of albumin in the blood, typically less than 30 g/L), generalised edema (swelling), hyperlipidemia (elevated levels of lipids, including cholesterol, in the blood), and an increased risk of venous thromboembolism.

60
Q

What are some causes of acute tubular injury/necrosis?

A

Acute tubular injury or necrosis can be caused by various factors, including ischemia (low blood pressure, sepsis, diarrhea/vomiting, bleeding) and toxins (drug-induced, antibiotics, chemotherapy, X-ray contrast agents).

61
Q

What is tubules’ sensitivity to ischemia in acute tubular necrosis cases?

A

Tubules are highly sensitive to ischemia, accounting for approximately 50% of cases of acute tubular necrosis.

62
Q

What is the pathophysiology of acute tubular necrosis (ATN)?

A

The pathophysiology of acute tubular necrosis involves several stages. It starts with the induction phase, the initial event leading to reduced glomerular filtration rate (GFR). This is followed by the extension phase, characterized by ongoing hypoxia, inflammatory response, and preferential involvement of the corticomedullary nephrons. Necrosis and cell death occur during this phase. In the maintenance phase, blood flow is restored, hypoxia is reversed, and cellular repair and proliferation take place. Finally, in the repair phase, tubular integrity is restored, leading to improvement in renal function.

63
Q

What are some common causes of interstitial nephritis?

A

Interstitial nephritis is characterized by inflammation within the mesangium of the kidney. It can be caused by various factors, including drugs (accounting for around 70% of cases) such as antibiotics, diuretics, and nonsteroidal anti-inflammatory drugs (NSAIDs). Infection (bacterial, viral, or fungal) and autoimmune disorders like systemic lupus erythematosus (SLE) and sarcoidosis can also cause interstitial nephritis.

64
Q

What are some examples of drugs with inherent nephrotoxicity?

A

Examples of drugs with inherent nephrotoxicity include aminoglycosides, cisplatin, contrast dye, cyclosporine, and amphotericin B.

65
Q

What are some common pathways through which drugs can cause renal damage?

A

Common pathways through which drugs can cause renal damage include altered intraglomerular hemodynamics (affecting blood flow within the glomerulus), tubular cell toxicity (direct toxicity to renal tubular cells), inflammation, crystal nephropathy (formation of crystals within the kidneys), rhabdomyolysis (breakdown of muscle tissue), and thrombotic microangiopathy (formation of blood clots in small blood vessels).

66
Q

What is acute kidney injury (AKI)?

A

Acute kidney injury is a rapid decline in excretory kidney function, characterized by a sudden decrease in glomerular filtration rate (GFR). It typically occurs over hours to days and is associated with the retention of nitrogenous and non-nitrogenous waste products and disturbances in electrolyte, acid-base, and fluid balance. AKI is present in approximately 1% of acute hospital admissions, and around 5% of hospitalized patients develop AKI.

67
Q

What are some common causes of acute kidney injury?

A

The causes of acute kidney injury can be classified into several categories. These include pre-renal causes such as hypovolemia (low blood volume), cardiac failure, and hepatorenal syndrome. Renal causes include renal artery occlusion, large/medium vessel vasculitis, small vessel disease (thrombotic microangiopathy, renal atheroembolism, small vessel vasculitis), glomerular diseases (anti-GBM disease, lupus nephritis, postinfectious glomerulonephritis, infective endocarditis, membranoproliferative glomerulonephritis, cryoglobulinemia, IgA nephropathy/Henoch-Schönlein purpura), acute tubular injury/necrosis (due to drugs, toxins, contrast agents, etc.), acute interstitial nephritis (caused by drugs, infections, systemic diseases), intra-tubular obstruction (cast nephropathy, drugs, crystalluria), and post-renal obstruction (papillary necrosis, tumors, retroperitoneal fibrosis, renal calculi, urinary retention).

68
Q

What are the treatment approaches for acute kidney injury (AKI)?

A

The treatment of AKI involves supportive care. The majority of cases require good quality supportive care alone. The specific treatment approaches depend on the underlying cause and clinical presentation. It is important to exclude life-threatening complications, identify the etiology of AKI, provide supportive treatment, and avoid factors that can worsen kidney function, such as nephrotoxic drugs.

69
Q

What are the indications for urgent renal replacement therapy in AKI?

A

Urgent renal replacement therapy, such as dialysis, may be required in certain situations. Indications for urgent renal replacement therapy include uncontrollable fluid overload, severe metabolic acidosis that cannot be controlled by other means, uncontrollable hyperkalemia (elevated potassium levels), uremic pericarditis or encephalopathy, and poisoning with substances such as ethylene glycol, lithium, or NSAIDs.

70
Q

What are some differences between acute and chronic renal failure?

A

Acute Renal Failure:

Patients are often acidotic and unwell.
Calcium levels are usually normal, unless there is an underlying cause.
Kidneys are typically of “normal” size.
Chronic Renal Failure:

Patients may surprisingly be well despite the condition.
Low calcium levels may be observed, along with renal osteodystrophy or hyperparathyroidism.
Kidneys appear small on ultrasound examination.
Kidneys may appear pigmented.

71
Q

What are the different options for renal replacement therapy?

A

Renal Replacement Therapy:
Haemodialysis: Involves the use of a vascular access (such as a dual lumen catheter or arteriovenous fistula) for blood purification outside the body. It is usually performed 3-4 hours, three times a week, either at home or in a dialysis center.
Peritoneal dialysis: Involves using the peritoneal membrane as a natural filter for waste removal. It can be performed at home and offers more flexibility.
Renal transplant: Involves the surgical transplantation of a healthy kidney from a donor into a recipient with kidney failure.

72
Q

What are some features of haemodialysis?

A

Haemodialysis:
It requires a vascular access, such as a dual lumen catheter or arteriovenous fistula.
The treatment typically lasts 3-4 hours, three times a week.
Haemodialysis can be performed at home or in a dialysis center.
It may have certain restrictions, such as during holidays or travel.

73
Q

What is peritoneal dialysis?

A

Peritoneal dialysis is a method of renal replacement therapy in which the peritoneum (the membrane lining the abdominal cavity) is used as the dialysis membrane. Electrolytes and toxins are exchanged between the peritoneal cavity and a dialysis solution, based on concentration gradients. Peritoneal dialysis typically involves 4-5 exchanges per day. Continuous Ambulatory Peritoneal Dialysis (CAPD) is a form of peritoneal dialysis that does not require a machine.

74
Q

What are some complications of peritoneal dialysis?

A

Complications associated with peritoneal dialysis include infection and blockage of the catheter. Infection, such as peritonitis, can occur due to contamination or poor catheter care. Blockage of the catheter can lead to inadequate dialysis and may require interventions to restore function.

75
Q

What are the options for kidney transplantation?

A

Kidney transplantation is a treatment option for end-stage renal disease. It can be performed using a live donor (such as a family member or compatible individual) or a cadaveric donor (deceased donor). The original kidneys are typically left in place during the transplantation procedure, and the transplanted kidney is usually placed in the right iliac fossa. Matching of blood type and tissue compatibility between the donor and recipient is crucial. Long-term immunosuppression is required to prevent organ rejection.

76
Q

What is maximum conservative treatment?

A

Maximum conservative treatment is a comprehensive approach to managing kidney disease that focuses on lifestyle modifications and medication. It includes interventions such as adopting a low sodium and potassium diet, reducing sugar intake, quitting smoking, controlling hypertension with medications like ACE inhibitors, managing diabetes effectively, and controlling cholesterol levels.

77
Q

What are some types of cystic renal diseases?

A

Autosomal Dominant Polycystic Kidney Disease (ADPKD): A genetic disorder characterized by the formation of multiple cysts in the kidneys, leading to their enlargement and potential impairment of kidney function.
Autosomal Recessive Polycystic Kidney Disease (ARPKD): Another genetic disorder characterized by the development of cysts in the kidneys, usually starting in early childhood. It can cause significant kidney and liver problems.
Simple cysts (Multicystic kidney): Fluid-filled sacs that form in the kidneys are usually benign and don’t cause significant health issues.
Cystic dysplastic: A congenital malformation of the kidney characterized by abnormal development of kidney tissue, resulting in the formation of cysts. It is usually unilateral (affecting one kidney).
Hydronephrosis: A condition characterized by the swelling of the kidneys due to the accumulation of urine, often caused by obstruction in the urinary tract. It can sometimes be mistaken for cysts.

78
Q

What is Autosomal Dominant Polycystic Kidney Disease (ADPKD)?

A

Autosomal Dominant Polycystic Kidney Disease (ADPKD) is a genetic disorder characterised by the development of numerous cysts in the kidneys. It is caused by an autosomal dominant mutation in the PKD1 gene located on the short arm of chromosome 16. This gene encodes for the Polycystin-1 protein, expressed in the cell membranes and cilia of tubular cells in the kidneys. ADPKD leads to a progressive increase in the size and number of cysts over many years, resulting in a gradual decline in renal function. It is usually asymptomatic with normal renal function until the third or fourth decade of life. Symptoms may include renal insufficiency, haematuria, hypertension, abdominal mass, and flank pain. The disease often progresses to end-stage renal failure, typically occurring in the seventh decade of life.

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What is Autosomal Recessive Polycystic Kidney Disease (ARPKD)?

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Autosomal Recessive Polycystic Kidney Disease (ARPKD) is a rare genetic disorder that follows an autosomal recessive inheritance pattern. Multiple small cysts characterise it in the renal cortex and medulla, which are radially oriented cysts of the collecting ducts. Individuals with ARPKD may also have multiple liver cysts and hepatic fibrosis. This condition is associated with pulmonary hypoplasia and typically presents in infancy with progressive and often fatal renal failure.

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What are simple renal cysts (multicystic kidneys)?

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Simple renal cysts, or multicystic kidneys, are acquired cysts in the kidneys. They are characterised by fluid-filled sacs with water density, thin walls, and no nodular or enhancing elements. It is important to differentiate simple renal cysts from cystic cancers to ensure accurate diagnosis and appropriate management.