Kidney Biopsy as a Consequence of Nephritic Syndrome

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The patient in question appears to present with raised blood pressure, reduced kidney function, and elevated serum creatinine, and the presence of blood and protein in his urine was revealed by a urine dipstick test. Initial assessment of the patient must comprise firstly of a detailed medical history including asking about symptoms he has noticed and how long they have been present in terms of changes in his urine output, colour, and other characteristics such as froth which suggests protein in the urine. Symptoms in other organs including skin disorders (like rashes), joint pain or hemoptysis can aid in the diagnosis of several autoimmune diseases with renal manifestations. Other symptoms like drowsiness and twitching could be the result of complications of kidney disease, caused by the inability of the kidneys to rid the body of metabolic waste products and their subsequent build-up.

Patients are also asked if they have any known diseases such as renal disorders, diabetes, systemic lupus or cancers or have recently had or been treated for an infection. Diseases such as polycystic kidney disease, nephritis and kidney failure could be inherited; hence a family history of any such disease could be of benefit. The patient’s drug history must also be taken into account, particularly of nephrotoxic drugs such as non-steroidal anti-inflammatory drugs (NSAIDs), lithium and penicillamine and even recreational drugs. Social and travel histories could reveal any possibility of an infectious cause for the patient’s symptoms. A physical examination of the patient would include assessment for fluid balance using features like skin turgor, JVP and oedema amongst other observations that could give clues such as hyperventilation being a possible indication of metabolic acidosis. Physical examination may sometimes be normal regardless of the presence of an underlying kidney disorder.

Glomerulonephritis (GN) is the acute or chronic inflammation of the glomeruli or glomerular capillaries in the kidneys and is assumed to be the cause of combined proteinuria and haematuria in the absence of leucocytes or nitrates in the urine; when an infectious cause can be excluded, until proved otherwise by further investigations. A repeat of the urine dipstick would help exclude the possibility of false positives due to functional causes of proteinuria such as exercise (Peggs et al., 1986), or as a result of concentrated or alkaline urine (Carroll and Temte, 2000) and similar causes for haematuria. Furthermore, the ability of a urine dipstick test to detect microalbuminuria (between 30 and 300mg/24 hours) or the presence of immunoglobulins, such as Bence Jones proteins secreted into the urine in disorders with renal implications like multiple myeloma or amyloidosis, is limited. To detect such proteins, alternative methods are required such as the sulfosalicylic acid turbidity test or immunofixation electrophoresis (2000).

Quantification of the protein excreted in the urine occurs through 24 hour urine collection, the “gold standard”, or is estimated by random protein to creatinine ratio (PCR), the latter of which was found in some, but not all, causes of GN to provide an accurate measure of protein excretion and more convenience for the patient (Kobayashi et al., 2019). The albumin to creatinine ratio (ACR) can also be used but is avoided in patients with nephrotic syndrome. The glomerular filtration rate (GFR) is used in practice as a reflection of kidney function, where any value higher than 60 ml/min/1. 73 m2 is considered in the normal range. The gold standard for accurate GFR measurement is inulin clearance since inulin is an exogenous substance that is freely filtered in the glomeruli and not reabsorbed or synthesised along the remainder of the nephron. This method of GFR measurement is avoided due to its complexity, large time-consumption and inconvenience to the patient and due to the limited availability of the substance and is saved for research when especially precise measures of GFR are required (Stevens et al., 2006). Instead, GFR is estimated in clinical practice by a formula using serum creatinine. Limitations of the latter approach include its variability amongst individuals due to muscle mass, diet and variable tubular secretion of creatinine (Traynor et al., 2006).

Microscopic urinalysis is subsequently used for further classification of the type of clinical presentation of glomerulonephritis. Red and white blood cells, epithelial cells, casts, crystals, bacteria and parasites can be detected and quantified, each providing a pointer towards the diagnosis. For instance, the presence of red blood cells could be an indication of glomerular damage. Had the patient been presenting with nephrotic syndrome, his urine dipstick test will have shown a markedly higher level of proteinuria (>3. 5 g/24 hours) than indicated and he would have shown hypoalbuminemia and hypercholesterolemia in his blood tests. Oedema would have likely been seen on physical examination of the patient. Nephritic syndrome is therefore more likely the case due to the presence of hypertension, haematuria and elevated creatinine levels alongside the observed deterioration in eGFR. Erythrocyte casts seen on microscopic urinalysis will also confirm nephritic syndrome, as well as reduced urine output reported by the patient. Acute kidney injury, for which acute illness, cardiovascular disease and diabetes mellitus are important risk factors, could worsen the condition and make it an emergency case, therefore it is essential to retrieve any information on these from the patient when taking a medical history, although this may be unlikely given the age of the patient and that he isn’t hospitalised. (Bucuvic et al., 2011) (Fenoglio et al., 2019).

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Further investigations aim to pinpoint the underlying pathological cause of the nephritic syndrome and will likely include a kidney biopsy, the gold standard for diagnosis of renal conditions. The sample taken can be visualised under a light (LM), electron (EM) or immunofluorescent microscope (IM). Imaging of the kidneys may also be useful and occurs through an ultrasound or CT scan. The latter is avoided in patients with impaired renal function due to the adverse effects of the injected dye not being cleared completely by the kidneys and can be as severe as cardiac arrest or kidney failure. Imaging techniques may reveal structural abnormalities in the kidneys such as polycystic kidneys or horseshoe kidney and kidney stones, masses or anything else that may be causing obstruction to urinary flow.

Causes of nephritic syndrome could be non-proliferative, where the number of cells remains constant, as in membranous glomerulonephritis in which a thickened basement membrane will be visible on the EM. Infections such as Hepatitis B and malaria and certain drugs could lead to this type of GN. Other proliferative causes, in which the number of cells increases, include Goodpasture’s syndrome or anti-glomerular basement membrane (GBM) disease, lupus nephritis and vasculitis, all of which are autoimmune disorders that reduced complement 3 and 4 levels in the blood can direct to in terms of diagnosis. In Goodpasture’s syndrome, anti-GBM antibodies that target the basement membrane of the blood vessels in the kidneys and lungs are found in blood tests and can be seen in the microscope in the case of renal involvement and immunoglobulin deposits can be seen under an IM. Lupus nephritis is a complication of systemic lupus erythematosus (SLE) and has five stages.

An antinuclear antibody (ANA) test can be used in its diagnosis. In small vessel vasculitis, autoantibodies called anti-neutrophil cytoplasm antibodies (ANCA) target neutrophils leading to blood vessel inflammation. This can be diagnosed by testing for ANCA in bloods or on the microscope after a biopsy, along with immune complex deposits in some cases on an IM. Finally, Immunoglobulin A (IgA) nephropathy, indicated by IgA deposits in the kidneys in an IM and elevated serum IgA, is the most common idiopathic cause of GN and occurs following certain infections. Another cause of nephritic syndrome could be post-streptococcal glomerulonephritis, characterised by the appearance of anti-streptococcal antibodies. Alport syndrome, diagnosed through electron microscopy of a kidney biopsy, is an inherited genetic disorder that surfaces as glomerulonephritis amongst other presentations and could be a cause of nephritic syndrome. All the differentials mentioned could lead to rapidly progressive glomerulonephritis (RPGN), in which the pathological findings are glomerular crescent formation and the presence of monocytes and macrophages (Couser, 1988). This subsequently progresses into end-stage renal disease (ESRD) within weeks or months.

Management of nephritic syndrome includes primarily controlling the patient’s blood pressure by means of angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARB). Hyperkalaemia is a serious complication of the use of such agents so potassium levels must be monitored. A calcium channel blocker is used instead in cases where the nephritic syndrome is a result of dehydration, due to the increased risk of AKI development. Immunosuppressants and steroids are used in cases of autoimmune aetiology behind renal disease. These agents possess overlapping side effects such as increased risk of infections, infertility and teratogenesis and cause changes in the patient’s physical appearance. In the case of RPGN, dialysis may urgently be required. As an invasive process, dialysis also makes the patient more prone to infection and delays the recovery of renal disease.

Chronic kidney disease (CKD) could result from the patient’s long-standing nephritic syndrome and is generally defined as an eGFR of less than 60 ml/min/1. 73 m2 for a minimum period of three months regardless of the presence of signs of kidney damage or having isolated evidence of kidney damage from laboratory and clinical tests, defined as an ACR greater than 30 mg/mmol or a structural renal abnormality revealed by imaging, regardless of eGFR (Levey et al., 2005). Regular testing is offered for patients at risk of developing CKD, such as diabetics and hypertensive patients or those with known kidney disorders like AKI or a family history of CKD. CKD can be classified into five stages based on reduction in eGFR, where stage 5 is known as end-stage renal disease (ESRD) and is when eGFR drops below 15 ml/min/1. 73 m2 and the patient will require dialysis and kidney transplantation.

In addition to eGFR, the ACR is used to stratify patients into three groups (A1-3) within each stage, where A3 represents the group with the greatest increase in ACR, above 30 mg/mmol, and the highest risk of progression to ESRD. In the case presented, the GFR of 49 ml/min/1. 73 m2 would be consistent with a diagnosis of stage 3a CKD, making him less likely to progress to ESRD and expected to have greater overall survival than patients with stage 3b CKD (Baek et al., 2012). The levels of an enzyme called cystatin C could be used at this stage to differentiate between ageing and CKD as causal factors for GFR reduction. The management of CKD aims to control symptoms and prevent common complications (Thomas et al., 2008). Initially, ACE inhibitors or ARBs are used to control blood pressure and reduce proteinuria. Limitations of treatment with such medications are that caution should be taken when used in renally impaired patients since they tend to reduce GFR and that they cannot be taken in combination with one another due to the increased risk of hyperkalaemia, a pre-existing complication of CKD. Blood glucose must be controlled in patients with diabetes.

Further complications of CKD include anaemia, which can be treated using erythropoietin if it is certain that the underlying cause is renal, whilst maintaining haemoglobin levels within the normal range to prevent strokes. Renal osteodystrophy, another possible complication, can be managed with calcium and Vitamin D supplements. Cardiovascular precautions are taken by giving patients statins and aspirin regardless of their age. In the case of progression to stage 5 CKD, renal replacement therapy in the form of either haemodialysis or peritoneal dialysis will be required to mimic normal renal function. Preferably, a kidney transplant can be done in which a donor kidney with the least possible number of tissue mismatches is used in an invasive surgical procedure, following the administration of steroids and immunosuppressants, each with their variety of side effects and possible complications, to prevent organ rejection.

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