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Renal biopsy (RBx) informs about kidney transplantation (KTx) prognosis. In our observational study the prevalence of histological anomalies and the prognostic role of CD45, vimentin (VIM) and periostin (POSTN) in KTx-RBx have been evaluated. One hundred forty-six KTx-RBx (2009-2012) were analysed for general histology and in immunohistochemistry for CD45, VIM and POSTN. Clinical data of the 146-KTx patients were collected at the RBx time (T0), 6 and 12 months before and after RBx. Follow-up time was 21 ± 14 months. Glomerulosclerosis was 20% glomeruli/biopsy. Tubular atrophy (TA), Interstitial infiltrate (I-Inf) and interstitial fibrosis (IF) were slight in 21–18% and 25%, moderate in 22–30% and 26% and severe in 30–18% and 28% of patients. Fifty-eight percent of patients had lesions compatible with IF-TA. CD45, VIM and POSTN correlated to each-other and to TA, I-Inf and IF. VIM and POSTN correlated to GS. CD45 and VIM correlated directly to renal function (RF) and 25(OH)VitD, while POSTN inversely to 25(OH)VitD. Thirty patients restarted dialysis (HD+). HD+ had lower T0-eGFR, and higher CD45, VIM and POSTN than HD−. POSTN resulted the strongest in discriminate for HD+ . CD45, VIM and POSTN correlate to each-other and predict graft outcome. POSTN was the strongest in discriminate for HD+. 25(OH)VitD might influence inflammation and fibrosis in KTx.

Secondary hyperparathyroidism (SHP) is one of the most challenging complications in the most advanced stages of end-stage renal disease. In the last decade, newly available medical tools have greatly increased the possibilities for controlling SHP. However, one of these tools, cinacalcet, has not yet been approved for its use in transplanted patients and the evidence for its safety in this clinical setting is still incomplete. For these reasons, many questions still remain open for the clinical nephrologist: when to consider a parathyroidectomy (PTX) in a patient on a waiting list for kidney transplant (KTx); when to recommend PTX after KTx; when could a regression of parathyroid hyperplasia be expected at any time after KTx. In the present paper, we will briefly deal with these questions in the light of an unusual clinical case.

The widely differing functions of vitamin D are based both on a wide diffusion of its specific receptor (VDR) and on the ability of many cells, in addition to renal tubular cells, to synthesize calcitriol for autocrine and paracrine functions. In the last few years, many published studies have added new insights into some important points on this topic. Recent data suggest that the control of calcitriol synthesis at tissue levels other than kidneys might differ greatly from the control system working at the renal level. Furthermore, the mechanisms by which the VDR might mediate either the genomic and nongenomic (rapid) vitamin D-mediated effects became much clearer. However, new evidence accumulated suggests that some additional receptor(s), responsive to vitamin D and different from the VDR, could play a role in the rapid response to vitamin D, probably interfering also with the genomic pathway. In this context, there are new possible interpretations of the mechanisms by which different vitamin D metabolites might express variable activities at different levels. In addition, some recent data have challenged the role of the VDR in direct parathyroid hormone (PTH) control, at least in physiological conditions, suggesting that vitamin D-mediated PTH inhibition is mainly secondary to the intestinal effect on calcium absorption. Finally, there is a renewed interest in the field of polymorphic variants in the VDR gene in relation to some clinical conditions, though the mechanisms underlining these associations are far from being clear. The present review briefly addresses all of the above points.

Despite a lot of research efforts, the origin of renal fibroblasts is still matter of debate. Epithelial-mesenchymal transition (EMT) of tubular epithelial cells could be at least one of the mechanisms by which renal fibroblasts are generated. Every kind of renal injury is potentially able to induce renal tubular cells to go through the various steps of EMT and generate fibroblasts, as it has been demonstrated by experimental models, in vitro experiments, and renal biopsy studies. It means that, if EMT is a common process of progression of renal failure, further studies and a better understanding of this process can lead us to envisage specific treatments to counteract the progression of renal disease.

Renal involvement in type 2 diabetes is a well known clinical occurrence. According to data from the literature, besides diabetic glomerulosclerosis, type 2 diabetic nephropathy may occur as a non specific chronic damage mostly related to vascular changes, or as a glomerular disease superimposed on or even unrelated to diabetic glomerulosclerosis. The most common picture remains in any case diabetic glomerulosclerosis (diabetic GS), that is characterized by variable degrees of mesangial sclerosis.

Henoch-Schonlein purpura is a clinical syndrome characterized by the association of skin, joint, and gastrointestinal symptoms. Henoch-Schonlein purpura is characterized by wide-spread vasculitis. Although the clinical symptoms of this disease are characteristic, the diagnosis is not always easy to establish because other forms of systemic vasculitis - mainly the microscopic form of periarteritis nodosa - may mimic the disease. In addition, in contrast to systemic lupus erythematosus, there are no biological tests that can identify Henoch-Schonlein purpura with certainty. Immunofluorescence microscopic techniques have made an important contribution to both the diagnosis and the study of the pathogenesis of the disease, particularly since they have demonstrated the presence of IgA deposits in the glomeruli and in the vessel walls. These findings not only confirmed the immunologic nature of the pathologic lesions but also drew attention to the remarkable similarity between Henoch-Schonlein purpura nephritis and IgA nephropathy.

Monoclonal diseases of B-cell lineage, often referred to as plasma cell dyscrasias, are characterized by abnormal and uncontrolled proliferation of a single clone of B cells at different maturation stages, with a more or less marked differentiation to immunoglobulin (Ig)-secreting plasma cells. Thus B-cell proliferation is usually associated with the production and secretion in blood of a monoclonal Ig or a fragment thereof. An ominous consequence of secretion of monoclonal Ig products is their deposition in tissue. These proteinaceous deposits can take the form of casts (in myeloma cast nephropathy), cristals (in myeloma-associated Fanconi's syndrome), fibrils (in light-chain [LC] amyloidosis), or granular precipitates (in monoclonal Ig deposition disease [LCDD]).

In the first part of Histopathological Atlas of Renal Diseases we described the typical morphological features of Anca-associated vasculitis. The histological features in Wegener's granulomatosis, Micropolyarteritis and its renal-limited variant, are characterized by "pauci immune" necrotizing extracapillary glomerulonephritis. The cellular composition of glomerular crescent and the mechanisms underlying crescent formation are still incompletely understood. The recent availability of monoclonal antibodies directed against epithelial cells and leucocytes allowed a more precise identification of the crescent cells. In this chapter we will describe the prevalent presence of monocytes in the crescents, the possible mechanisms of recruitment of these cells and the morphological consequences of this glomerular infiltration for the chronic progression of lesions.

"ANCA-associated vasculitis" are Wegener's Granulomatosis, Micropolyarteritis and its renal-limited variant (previously called idiopathic necrotizing glomerulonephritis). According to the "Chapel Hill Consensus Conference" classification, ANCA-associated vasculitis are characterized by prevalent involvement of small-size vessels, whereas medium and large-size arteries involvement is the marker of Polyarteritis Nodosa. But the vessel size-based classification is not always powerful enough, because also in ANCA-associated vasculitis the involvement of medium and large-size arteries if frequent. The distinctive marker of ANCA-associated renal vasculitis has therefore become the presence of necrotizing extracapillary glomerulonephritis, that is always absent in Polyarteritis Nodosa.

Minimal Change disease and focal segmental glomerulosclerosis are both clinically characterized by presence of Nephrotic Syndrome. The term Minimal Change disease describes a pathology appearance on light microscopy in which there are no definitive changes from normal glomeruli, although the degree of change that is considered significant remains the subject of some controversy. The focal segmental glomerulosclerosis is morphologically characterized by a segmental solidification of the glomerular tuft, due to collapse of the capillary wall, affecting only some glomeruli (focal). It remains unresolved whether Minimal Change disease and focal segmental glomerulosclerosis are different diseases or whether they represent a spectrum of presentation of the same disease process.

Acute post-streptococcal glomerulonephritis, also known as "proliferative-exudative nephritis" is morphologically characterized by intense endocapillary proliferation and massive accumulation of inflammatory cells.

Membranous glomerulonephritis (MGN) is characterized by thickening of the glomerular basement membrane due to the presence of subepithelial immune deposits. From a morphological point of view, idiopathic MGN is indistinguishable from class V lupus nephritis. The glomerular lesion is extremely variable and the basement membrane thickening changes over time. According to the classic descriptions, MGN is in fact divided into four stages.

Membranoproliferative glomerulonephritis (MPGN) is histologically characterized by intense glomerular hypercellularity (mainly due to mesangial proliferation) and diffuse thickening of the glomerular basement membrane with the appearance of ""double contours"". Two distinct histological forms have been identified--Type I MPGN and Type II MPGN. Type I MPGN is characterized by the predominant presence of subendothelial deposits, while Type II MPGN presents dense homogenous deposits in the basement membrane. Actually, despite many morphological and clinical similarities, there are enough histological and immunohistological differences to suggest that Type II MPGN is a separate and distinct entity, caused by different pathogenetic and morphogenetic mechanisms. Some researchers have identified a further entity: Type III MPGN, characterized by the concomitant presence of subendothelial and subepithelial deposits, but many authors at present believe that Type III MPGN is a morphological variant of Type I MPGN, given their clinical, immunological, and immunohistological similarities

The characteristic and diagnostic lesion of idiopathic IgA nephropathy (IgAN, Berger's disease) is glomerular IgA deposition, as a unique or predominant positive immunoglobulin. Despite the relatively uniform feature of the immunohistological pattern, the morphological lesions observed by light microscopy are extremely variable. This variability in glomerular and interstitial alterations has frequently created some difficulties in histological classification.