​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.

Pathology - Acute Tubulointerstitial Nephritis brought on by Drugs
Pathophysiology 
This patient has acute tubulointerstitial nephritis (ATIN) brought on by drugs.
Echogenic kidneys of normal size found on ultrasonography are consistent with parenchymal inflammation, as is the presence of white cell casts and eosinophiluria, which are markers of inflammation. Urinary glucose squandering in the presence of normal serum glucose and the absence of hematuria or proteinuria in this instance indicate tubular illness rather than glomerulopathy. Notably, there is no temperature and a negative urine culture, indicating that renal inflammation is not being caused by a urinary tract infection. ATIN is frequently brought on by an infection or a medication allergy. Antibiotics, NSAIDs, and more lately PPIs—this patient is taking both amoxicillin and a PPI, which are both linked to ATIN—are among the medications that are frequently to blame. A conclusive test would be a renal biopsy, which would typically reveal inflammatory cells infiltrating the renal parenchyma while sparing the glomeruli. Drug withdrawal is the first line of treatment, followed by supportive management and observation. If the first treatment doesn't work, the following measures are a renal biopsy and steroid therapy.

​Pathology - Urinary Tract Infection 
​Pathophysiology 
Recurrent infections have led to the development of chronic pyelonephritis. The agent is confirmed to be E. coli by a urine culture, as is typically the case in community-acquired UTIs.
Getting a sexual history is crucial in order to rule out urethritis brought on by an STD. Urgency, frequency, and dysuria are signs of lower urinary tract involvement. Fever and flank pain are signs that the infection has progressed up the ureters and into the renal pelvis, where it has caused pyelonephritis. Although the issue is bilateral in this instance, it is typically unilateral. Tubular injury is indicated by the presence of hyperkalemia, ketoacidosis, and isosthenuria (low urine concentration or dilution). Renal scarring results from persistent or recurrent infections (small kidneys on ultrasonography), and interstitial fibroblasts, inflammatory cells, and substantial tubular loss are predicted findings in a biopsy.

​Pathology - Chronic Kidney Disease 
Pathophysiology 
Based on eGFR, there are five stages of the disease; she is in stage 4, which denotes renal failure, with a GFR of less than 15. In 45% of cases, a complication of diabetes mellitus is the most common cause; untreated hypertension, like the one in this instance, is the second most common reason.

Nephron mass gradually decreases as a result of chronic kidney disease, regardless of the underlying reason. Renal ultrasound shows that the kidneys are tiny and fibrosed in the majority of cases. Patients can experience up to 70% nephron loss and still be asymptomatic due to hyperfiltration in the remaining nephrons. Hyperfiltration, however, damages glomeruli and hastens the loss of more nephrons.

​Fatigue and malaise are linked to anemia caused by a decrease in renal erythropoietin (EPO) output. Uremia and acidosis, which cause widespread metabolic disruption, exacerbate this. In this instance, fluid overload brought on by a loss of renal excretory capacity is contributing to the hypertension; heart failure symptoms are not yet evident. Metabolic acidosis and elevated serum phosphate and potassium are also caused by a loss of renal excretion. Reduced intestinal calcium absorption and a drop in blood calcium are caused by a loss of renal vitamin D activation. (In a different situation, the metabolism of calcium and phosphate in renal illness is covered in more detail.) Prior to renal dialysis and transplantation, patients should receive nutritional support to reduce their intake of salt, potassium, and phosphate from food, restrict their protein intake, and refill their vitamin D and EPO levels.

​Pathology - Hypovolemia 
Pathogenesis 
A drop in ECF volume is reflected in hypovolemia. Orthostatic hypotension is caused by insufficient blood volume, while tachycardia is a result of the SNS being activated by the arterial baroreceptors. The absence of a discernible jugular vein pulse signifies a reduction in the volume of venous blood, as 70% of blood typically stays in systemic veins. Common symptoms of hypovolemia that are mediated by the central nervous system include thirst and salt cravings. Internal fluid changes (also known as "third spacing") or fluid loss from the gastrointestinal tract, kidneys, or integument are common causes of volume depletion. It's crucial to remember that electrolyte imbalances do not indicate volume depletion. For instance, in hypovolemic patients, the concentration of sodium can be elevated, lowered, or normal as a result of water balance. In this instance, isotonic saline infusion cures secretory diarrhea, which causes a proportionate (isotonic) loss of salt and water.

​Pathology - Silicosis
Pathophysiology 
 Inhaling crystalline silica dust causes this long-term inflammatory lung parenchyma disease. The majority of individuals experience a notable lag time between exposure and the start of symptoms.
The presence of silica dust in terminal respiratory units triggers the production of distinctive "onion skin" nodules on radiographs, as well as cytokine and macrophage responses. Fibroblast activation follows. Compared to general populations, these patients are far more prone to mycobacterial infections, and TB diagnoses can be made alongside silicosis diagnoses.
In this patient, end-stage fibrosis is the cause of the fine rales. Spirometry results showing reduced total lung capacity and vital capacity are consistent with restrictive lung fibrosis. These patients typically maintain measurements that are more sensitive to big airway illness, such as the FEV1/FVC ratio.