4. Renal diseases identified by biopsy

Glomerular diseases require the visualization of light microscopy to best understand the numerous entities, many of which have similar immune-mediated pathophysiology. There are nine main light microscopic patterns. Each has a primary and secondary form. This classification allows one to understand the differences of 18 different confusing entities. These patterns are nil lesion, diffuse membranous, diffuse proliferative, diffuse membranoproliferative, focal proliferative, focal sclerosis, nodular glomerulosclerosis, fibrillary, and amyloidosis. For almost everyone, there is a primary and secondary form. The primary forms are idiopathic. The secondary forms are due to a bacteria or virus, a drug, or a systemic disease such as lupus. Based on the light microscopy, the clinician determines if there is a definite cause or whether it is primary. From either category a specific management has reached consensus by nephrologists through international symposia and guidelines.

Tubular diseases do not often show azotemia early. Rather subtle electrolyte findings such as hyperkalemia, hyperuricemia, or non-anion gap metabolic acidosis suggest this category of disease. However, since those disturbances can occur with nonrenal diseases such as gastrointestinal problems, they are not often recognized as early signs of renal damage. Renal biopsy helps distinguish the following most common causes: obstructive or reflux nephropathy, hypertensive injury called acute or chronic nephrosclerosis, drug-induced diseases such as due to analgesics, heavy metal injury such as due to lead, crystal diseases such as urate or oxalate, and unknown causes such as Balkan or other environmental nephritides.

Vascular diseases may occur with or without glomerulonephritis. Fibrinoid necrosis, chronic hypertensive changes of the arteries (nephrosclerosis), and vasculitis are the most common patterns. Fibrinoid necrosis is seen with malignant hypertension, thrombotic thrombocytopenic purpura, scleroderma, eclampsia, and disseminated intravascular coagulation.

Interstitial diseases are identified by acute and chronic inflammatory cells or fibroblasts and collagenous scarring between the tubules causing secondary tubular injury and renal failure. Chronic allograft nephropathy and chronic pyelonephritis are two examples.

### 5. Conclusion

The above framework to be used for the management of patients with chronic unexplained or understood renal insufficiency is frequently changing. New entities are appearing to add more patterns, more secondary causes of glomerular diseases, and new algorithms for management [5, 6]. Renal disease due to human

### Introductory Chapter: Renal Diseases DOI: http://dx.doi.org/10.5772/intechopen.90067

3. Renal biopsy

Renal Diseases

tory cells or scarring by fibrosis between them.

4. Renal diseases identified by biopsy

disseminated intravascular coagulation.

are two examples.

5. Conclusion

2

Normal renal histology must be known to the clinician before biopsy can be interpreted. The glomeruli will be numerous and have wide-open, thin-walled capillary loops; no inflammatory cells seen; and no increase in numbers of

mesangial cells. There can be less than 30% of any glomerulus or all glomeruli which contain amorphous loss of architecture called sclerosis. The blood vessels need to be open without cellular or muscular thickening. Finally, the cross section of renal tubules normally abuts directly against each other without evidence of inflamma-

Glomerular diseases require the visualization of light microscopy to best understand the numerous entities, many of which have similar immune-mediated pathophysiology. There are nine main light microscopic patterns. Each has a primary and secondary form. This classification allows one to understand the differences of 18 different confusing entities. These patterns are nil lesion, diffuse membranous, diffuse proliferative, diffuse membranoproliferative, focal proliferative, focal sclerosis, nodular glomerulosclerosis, fibrillary, and amyloidosis. For almost everyone, there is a primary and secondary form. The primary forms are idiopathic. The secondary forms are due to a bacteria or virus, a drug, or a systemic disease such as lupus. Based on the light microscopy, the clinician determines if there is a definite cause or whether it is primary. From either category a specific management has reached consensus by nephrologists through international symposia and guidelines. Tubular diseases do not often show azotemia early. Rather subtle electrolyte findings such as hyperkalemia, hyperuricemia, or non-anion gap metabolic acidosis suggest this category of disease. However, since those disturbances can occur with nonrenal diseases such as gastrointestinal problems, they are not often recognized as early signs of renal damage. Renal biopsy helps distinguish the following most common causes: obstructive or reflux nephropathy, hypertensive injury called acute or chronic nephrosclerosis, drug-induced diseases such as due to analgesics, heavy metal injury such as due to lead, crystal diseases such as urate or oxalate, and

unknown causes such as Balkan or other environmental nephritides.

Vascular diseases may occur with or without glomerulonephritis. Fibrinoid necrosis, chronic hypertensive changes of the arteries (nephrosclerosis), and vasculitis are the most common patterns. Fibrinoid necrosis is seen with malignant hypertension, thrombotic thrombocytopenic purpura, scleroderma, eclampsia, and

Interstitial diseases are identified by acute and chronic inflammatory cells or fibroblasts and collagenous scarring between the tubules causing secondary tubular injury and renal failure. Chronic allograft nephropathy and chronic pyelonephritis

The above framework to be used for the management of patients with chronic unexplained or understood renal insufficiency is frequently changing. New entities are appearing to add more patterns, more secondary causes of glomerular diseases,

and new algorithms for management [5, 6]. Renal disease due to human

immunodeficiency virus, new drugs including new biologicals, and new immunologic diseases accounts for some of these newer entities.

In conclusion, a word should be said about repeat renal biopsies. Repeat biopsies are encouraged to assess response to treatment such as in allograft rejection. Repeat biopsies are used to reassess those diseases such as lupus nephritis which can change course leading to new pathophysiology and demanding a change in therapeutic strategy.

Finally, the group at New York Presbyterian/Columbia University Medical Center should be commended as they have continued to provide the most comprehensive annual tutorial and update of the interpretation of renal biopsies based on the very large number of biopsies referred to them [7]. Many of the chapters in this book concentrate on the importance of renal biopsy for diagnosis. Other chapters deal with methods of performing renal biopsy. Finally, there are chapters dealing with complications of renal biopsy.
