​Pathology - Secondary Hypertension
Pathophysiology 
Like in this instance, secondary causes of hypertension usually present with a more sudden start, are more severe, and are more challenging to treat medically than essential hypertension. One significant factor that causes reduced renal blood flow and the activation of the renin-angiotensin-aldosterone pathway, which leads to salt and water retention, is stenosis of one or both renal arteries. The absence of bruit detected during auscultation is incompatible with this reason, and low renin levels and medical imaging both ruled it out. High aldosterone levels imply primary hyperaldosteronism (Conn syndrome), with renin levels regulated by negative feedback. Aldosterone stimulates renal tubular potassium and hydrogen ion release into the urine, which results in hypokalemia and alkalosis. When adenomas are less than 0.5 cm, like in this instance, they may not show up on CT imaging due to uncontrolled aldosterone secretion.
Primary hyperaldosteronism has multiple origins, such as idiopathic hyperaldosteronism, cancer, adrenal hyperplasia, and adenomas. Secretory masses are surgically excised, and aldosterone antagonists are used as a medicinal treatment for the latter.

​Pathology -Clostridium difficile Infection 
Pathophysiology 
Acute diarrheal illness is a very prevalent condition with a wide range of both infectious and noninfectious causes. Increased intestinal fluid output, decreased fluid absorption, increased motility, and increased luminal osmolarity are common mechanisms of diarrhea. Viruses (such as noroviruses and rotaviruses), bacteria (such as Shigella, Salmonella, Campylobacter, Yersinia, Clostridium, Listeria, Vibrio, and E. coli), protozoa (such as Giardia, Cryptosporidium, and Entamoeba), and fungi are examples of common infectious agents. Infection with C. difficile is the most frequent cause of hospitalized patients' symptoms. Previous antibiotic treatment disturbs the healthy gut flora, which gives C. difficile a chance to colonize the colon. Toxins A and B, which are produced by this gram-positive, spore-forming bacillus, harm the colonic epithelium and result in colitis and the development of gray pseudomembranes. The gold standard for diagnosis is the C. difficile cytotoxin stool sample assay. Vancomycin or metronidazole can be used to treat this illness. Although the clinical course varies, severe cases may lead to a toxic megacolon that is potentially fatal.

​Pathology - Renal damage and nonsteroidal anti-inflammatory drugs
Pathophysiology 
This is exceedingly uncommon in euvolemic individuals with normal renal function, but it is much more common in patients with hypertension or chronic kidney disease (CKD) and those with pre-existing risk factors such as states of decreased effective circulation volume. Angiotensin II, vasopressin, and renal sympathetic nerves all have vasoconstrictor and antinatriuretic effects; renal prostaglandins operate as local counterregulatory hormones to counteract these effects.
In euvolemia, their activity level is minimal, but when the effective circulatory volume is low, they play a crucial compensatory role in maintaining renal blood flow and glomerular filtration. In addition to taking high doses of an NSAID, which caused renal vasoconstriction and increased tubular salt retention, this patient has a history of hypertension, which puts them at risk. A pre-renal pattern with a BUN:creatinine ratio larger than 20 is caused by elevated serum creatinine and BUN. Reduced renal excretory function leads to fluid retention, which exacerbates hypertension again, and water retention, which results in hyponatremia. Inadequate excretion of hydrogen and potassium ions results in hyperkalemia and metabolic acidosis.
When combined with the absence of renal tubular cells in the urine sediment, low urine sodium excretion suggests enthusiastic tube absorption and indicates that the patient has not advanced to ATN. Imaging shows the absence of any obstructing processes. The goal of treatment is to stop taking NSAIDs; if this happens, the issue should resolve on its own.

Pathology - Hepatorenal Syndrome 
Pathophysiology  
 Arterial underfilling lowers renal perfusion pressure, which compromises renal function. Renal blood flow and glomerular filtration are reduced when renal vasoconstriction and renal blood flow occur together. Because of elevated amounts of vasodilators such nitric oxide, liver cirrhosis results in broad systemic vasodilation and blood pooling in the splanchnic circulation. Reduced diastolic blood pressure results in hyperdynamic circulation, tachycardia, and a broad pulse pressure (also observe the systolic flow murmur). Vasopressin secretion and the renin-angiotensin-aldosterone axis are stimulated by a decrease in the effective circulation volume. Renal vasoconstriction and sodium retention (urinary Na <10 mEq/L) follow as a result. Renal sympathetic efferent nerves and hepatic afferent nerves are also activated, causing a hepatorenal reflex that intensifies renal vasoconstriction.

​Peritonitis, GI hemorrhage, over-diuresis, or, in this case, large-volume paracentesis are examples of second insults to the circulation that frequently set off the hepatorenal syndrome's progressive and fatal renal failure. Other organic kidney diseases must be ruled out in order to make a diagnosis (notice the normal renal ultrasonography and inactive renal sediment). The only long-term, effective treatment is a liver transplant, and the prognosis is quite bad.

Pathology - Obstructive Uropathy 
​Pathogenesis 
In this instance, persistent bladder outlet obstruction has been caused by urethral stricture, a frequent condition in older men (notice bladder wall thickening). A urinary tract infection has resulted from urinary stasis (notice urine culture and fever). Urine retention and elevated pressure in the urine collection system due to bladder obstruction result in hydronephrosis, which is characterized by dilatation of the renal pelvis and calyces. GFR declines as a result of decreased net ultrafiltration pressure brought on by increased back pressure in the nephron and Bowman's space. A reduction in potassium and hydrogen ion release as a result of impaired distal tubular performance leads to metabolic acidosis and hyperkalemia.
The goal of treatment is to remove the obstruction—in this case, the urinary tract infection—as soon as possible. The degree and length of blockage determine how much renal function recovers. Long-term catheter use is not preferred over definitive therapy, such as surgically removing tumors, stones, the prostate gland, etc.

​Pathology - Minimal Change Disease 
Pathophysiology 
Generally speaking, nephrotic syndrome is a noninflammatory glomerulopathy in which albumin and other tiny serum proteins are able to pass through the glomerular filtration barrier. Numerous factors can lead to nephrotic syndrome, such as certain glomerulopathies, infections, cancer, and systemic illnesses like lupus. Urinary albumin loss causes edema by lowering serum albumin concentration, which in turn lowers plasma oncotic pressure.
Nephrotic syndrome can also cause other general complications, such as hyperlipidemia from disordered lipid processing, thrombosis from loss of urine anticlotting factors, infection from loss of immunoglobulin, and iron-resistant anemia from loss of transferrin. As in this instance, minimal change illness is the most common cause of nephrotic syndrome in children. Circulating factors that damage the filtration membrane are thought to be of lymphoid origin. The absence of glomerular abnormalities in biopsies examined under light microscopy gives rise to the disease's name. Most cases of corticosteroid treatment result in remission.

Pathology - Primary Focal Segmental Glomerulosclerosis 
Pathophysiology 
Has been linked to nephrotic syndrome. Because of the high rate of urine protein loss, alterations in capillary Starling forces result in hypoalbuminemia and the production of edema. This patient has primary (idiopathic) focal segmental glomerulosclerosis (FSGS), a condition in which podocyte abnormalities and glomerular filtration barrier failure are caused by circulating immunological stimuli or genetic disorders. The high rate of progression to end-stage renal disease makes the FSGS damage pattern observed on biopsy significant. Numerous secondary causes of FSGS exist, such as infections, nephrotoxins, cancers, and systemic disorders. The patient's medical history excludes a few typical secondary causes. "Membranous nephropathy" (MN), in which the glomerular basement membrane is observed to be thicker on light microscopy and immunostaining would reveal IgG deposition throughout the glomerular capillary loop, is another common appearance on renal biopsy of patients with nephrotic syndrome. Electron microscopy in the instance of MN would demonstrate that the thickening of the basement membrane was caused by sub-epithelial deposits and that the podocyte foot processes had been visibly effaced. MN may arise from multiple secondary causes or from a primary autoimmune disease.
​Nonimmunotherapies such a low-salt diet, diuretics to alleviate edema, ACE inhibitors to lower intraglomerular blood pressure (by dilatation of efferent arteriole), and lipid-lowering medications are generally used in the treatment of nephrotic syndrome.
When MN is present, immunosuppression may also be employed.

Pathology - ​IgA Nephropathy
​Pathophysiology 
Renal failure and an intraglomerular inflammatory process are the hallmarks of the nephritic syndrome. Hematuria and variable proteinuria are usually seen. Hematuria is the cause of dark brown urine. Red cell casts and dysmorphic RBCs both suggest that hematuria has a glomerular origin. Red blood cells that have crossed the glomerular basement membrane exhibit dysmorphic changes. Red blood cells and the Tamm-Horsfall protein in the tubule combine to generate RBC casts. There are numerous causes of nephritic syndrome; however, in general, the inflammatory process can be brought on by antibodies attaching to glomerulus structures (such as the basement membrane), by circulating immune complexes that accumulate in the glomerulus, or by deposited antigens that precipitate inflammation. One instance of an immune complex forming in the bloodstream is IgA nephropathy, which is assumed to be caused by faulty IgA molecules that self-aggregate. Episodes differ in timing from traditional post-streptococcal glomerulonephritis, in which hematuria appears one to two weeks after infection, and frequently co-occur with upper respiratory tract infections. The traditional tetrad of symptoms—rash, joint pain, abdominal discomfort, and hematuria—is experienced by certain IgA nephropathy patients. Henoch-Schönlein purpura, a more widespread form of IgAdominant vasculitis, is the ailment in question.

​Pathology - Membranoproliferaitve Glomerulonephritis
The patient is suffering from MPGN, or membrane proliferative glomerulonephritis.
Although there are differences in the severity of presentation, hypertension and a certain level of reduced renal function are frequently present. In this instance, nephrotic syndrome—which causes protein loss and edema—combines with nephritis, resulting in blood in the urine of glomerular origin. Uninterrupted complement cascade activation within the glomerulus is the source of inflammation.
The immune complex deposition or anomalies of the complement's inhibitory regulatory components can start the cascade. Therefore, the condition's hallmark is serum complement depletion. Crescent formation is a sign of more advanced illness and results from cellular growth in Bowman's space, which compresses the functioning filtration membrane. MPGN can be secondary, frequently associated with a history of hepatitis C infection, or primary (idiopathic), for which the origin is unknown. Based on the location of dense deposits on electron microscopy, three types of MPGN are identified: Type I, which is subendothelial and mesangial as in this instance; Type II, which is intramembranous within the glomerular basement membrane; and Type III, which is subendothelial, mesangial, and subepithelial. A distinct complement activation profile is linked to each variation.

​Pathology - Anti-glomerular Basement Membrane Disease, or Goodpasture Syndrome
Goodpasture syndrome, another name for anti-glomerular basement membrane illness, is a condition in which autoantibodies are produced against a type IV collagen antigen and cross-react with both the pulmonary alveoli and the glomerular basement membrane. This is known as Goodpasture syndrome when there is acute damage to both the kidney and lung, as it is in this case.
It is more likely in older people to experience isolated renal involvement. Although the exact cause of autoimmunity is unknown, an infection may be the catalyst; HLA DR15 and DR4 positive people are more susceptible. The majority of cases of hemoptysis are in smokers. The vital signs of this patient show a substantial pulmonary hemorrhage. Rapid and potentially lethal pulmonary bleeding and renal function decrease are possible outcomes. The staging of renal crescents on biopsy is important because it demonstrates that, as opposed to growing gradually from a different cause, they all formed at the same moment the anti-GBM antibodies first appeared. The glomerular basement membrane likewise exhibits a linear pattern when stained with immunofluorescence. Before the invention of immunosuppressive medications and plasma exchange, the prognosis for Goodpasture syndrome was extremely bad.